On 2020-06-23 10:31:41, user OxImmuno Literature Initiative wrote:

https://www.immunology.ox.a...

On 2025-09-03 15:18:41, user Navaz Davoodian wrote:

Thank you for sharing this manuscript. The association between outdoor night-time light exposure and Alzheimer’s disease (AD) is important, but the findings should be framed as correlational, not causal. Areas with higher light pollution typically coincide with greater urbanicity—higher population and building density—alongside air and noise pollution, heat-island effects, socioeconomic differences, healthcare access, and greenspace deficits. These co-exposures could confound the observed relationship, as could diagnostic/detection bias (urban areas may identify AD more readily).

Exposure assessment based on ambient/satellite light also may not reflect individual night-time exposure (bedroom light levels, spectral content, window treatments, indoor lighting, time–activity patterns). I suggest: (i) tempering causal language throughout; (ii) adjusting more fully for urban co-exposures (e.g., PM2.5/NO2, noise, heat, SES, greenspace) with sensitivity analyses and spatial terms; (iii) exploring plausible mediators (sleep/circadian disruption) and effect modifiers (age, sex, SES); and (iv) noting the need for longitudinal cohorts with personal light dosimetry and actigraphy. As it stands, the study demonstrates a relationship between artifacts of urbanity (of which night-time light is one) and AD, rather than a direct effect of lighting per se.

On 2021-03-10 11:48:29, user Erick wrote:

The percentage of participants who were female was Group 3 > Group 2 > Group 1, and women were shown to have more robust response than men to the infection and the vaccines. Based on this, what was the prior probability that the result obtained here would be due to the differing proportions of female/male in the three groups? Was the p-value adjusted for this or a test done to ascertain the Sex-effect?

What was the evidence presented to support conclusion (b) about the vaccine prioritization? Seems a lot of factors go into that decision than addressed here.

On 2019-06-28 18:46:32, user hkahn wrote:

Congratulations on an ambitious study design. It would be great to have also a comparative cohort sampled from the general adult population, but that would be very costly. Perhaps you could attempt parallel analyses from the EPIC population cohorts in Germany.

ANTHROPOMETRY:<br /> I didn't find many details, but surely the standing waist circumference (WC by the WHO protocol) will be included. I urge BeLOVE to consider adding the supine sagittal abdominal diameter (SAD) to the phenotyping assessments. The SAD has been quickly, reliably measured by a portable sliding-beam caliper (http://www.cdc.gov/nchs/dat... "http://www.cdc.gov/nchs/data/nhanes/nhanes_13_14/2013_Anthropometry.pdf)"). Studies in Sweden, Finland, India, Taiwan, Brazil, USA have demonstrated that SAD can serve to estimate the amount of visceral (intra-abdominal) adipose tissue. The supine SAD usually performs better than WC to identify dysglycemia, dyslipidemia, transaminase elevations, and hypertension. Since your participants will be supine for portions of the CRU assessment, you could inexpensively add the caliper measurement at that time.

Your SAD values by the low-cost caliper could be compared with the more costly dimensions and VAT area (or volume) estimates extracted from your supine abdominal imaging.

Population-based normative values for adult SAD are now available from Finland (Health 2000 Study) and from NHANES (2011-2016) in the USA. They confirm that SAD increases with age and tends to be larger for men than women.

The indicator SAD/height ratio (SADHtR) yields values that are nearly identical for men and women; thus, SADHtR can be evaluated as a risk estimator for men and women (just as the BMI purports to serve for men and women equally). Population norms for SADHtR are available from Finland and the USA. From the initial 4 years of NHANES we have demonstrated that SADHtR is superior to WHtR (and much superior to BMI) for identifying adults with insulin resistance (HOMA-IR), hypertriglyceridemia, and increased values of Tg/HDLc or the TyG index (https://www.ncbi.nlm.nih.go... "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6003239/)").

I hope these thoughts will contribute to the success of the BeLOVE Study.

On 2020-04-28 13:51:34, user alasdair hay wrote:

I am not convinced this paper provides any evidence on the safety of HFNC in respiratory infections. My understanding is the study shows similar number of respiratory particles were measured in all conditions from breathing air to any 02 device or coughing.

I would be more reassured if the articlce demonstrated an increased number of respiratory aerosol particles with some airway devices or proccedures but not HFNC. In fact there is no control demonstrating the SMPS aerosol measurement probe detects respiratory droplets. The only particles the probe appeared to detect were produced by a candle. If the probe is picking up a background number of particles in the air and those produced by a candle it is not picking up anything of medical interest

On 2020-06-04 16:36:04, user Rosemary TATE wrote:

Unfortunately the complicated modelling approach and poorly labelled graphs makes this potentially interesting article difficult to understand. There is no mention of limitations in the discussion section (see STROBE guidelines). Two obvious ones are 1. The progress of covid is different in different countries, so some countries will have lower cases just because the pandemic started later there 2. The data is very variable between countries and is dependent on how well they record covid deaths, so may not be reliable.

On 2021-02-09 09:47:38, user Alex wrote:

Hi guys, interesting paper. I’m curious as to how you justified a change in well-being pre-during when baseline data was collected during the peak?

On 2021-08-18 03:09:54, user jasonchouinard wrote:

Great comment and idea. I am here from the blog at Merogenomics.ca

Concerning viable viruses the authors of this study state, "We did not evaluate viability of shed virus via viral culture." From a systematic review and meta-analysis of 79 studies (5340 individuals) on SARS-CoV-2, eight studies (1858 individuals) on SARS-CoV, and 11 studies (799 individuals) on MERS-CoV: https://www.thelancet.com/j... we can learn that, "No study detected live virus beyond day 9 of illness, despite persistently high viral loads, which were inferred from cycle threshold values."

So from the Figure 1 Scatter plot, we can see in the first four days that vaccinated people are indeed slightly lower Ct/higher supposed viral load, when 28% were also asymptomatic in this dangerous time of transmissibility. So from the study, should "Vaccinated individuals had a more rapid decline in viral load, which has implications on secondary transmission and public health policy," be changed to show/reflect/warn that Vaccinated individuals are slightly more transmissible and more likely to be asymptomatic during this dangerous time (more so than Unvaccinated) and in all likely hood both groups would be non-transmissible by nine days (or and appropriate TCID50/mL before that) so PCR testing is a moot point re: transmission/infection?

On 2020-04-27 11:07:45, user Pilar Domingo Calap wrote:

We have detected a small factual error in the text. The sentence containing the error is the following:

"The first confirmed case in the Iberian Peninsula was communicated on February 24, 2020 in Burriana, a small town nearby the city of Valencia, followed by another case the following day in Valencia."

This sentence should be instead be:

"The first three confirmed cases in the Iberian Peninsula were communicated on February 25, 2020 in Madrid, Barcelona, and Villareal, a small town nearby the city of Valencia."

Pilar Domingo-Calap (co-author of the preprint)

On 2021-02-02 18:17:42, user Robert Enger wrote:

The #1 candidate is "cook". Frequently that person stands in proximity to the grill, which is a high air flow location, due to the high power exhaust fan system in the range-hood over the grill. This acts as a funnel, sucking air from the kitchen (and surrounding areas back to the various points of makeup-air ingress). The cook is thus "downstream" from numerous co-workers in the kitchen, and from persons in other locations between the makeup-air ingress points and the range hood (potentially all the restaurant patrons, if interior dining resumes).

This should sound familiar. Recall the studies of remote distance Covid transmission studied in Korea and China. In those studies, high air flow from air conditioner output ports carried virus from infected individuals to victims many feet removed from the infected party. In this case, the cook near the range-hood is "downstream" from potentially significant numbers of individuals (depending on the location of makeup-air ingress points, etc).

If this line of reasoning is found to be sound, then providing a direct ingress path for outside fresh air to enter into the kitchen "may" reduce the exposure of the cook (and nearby kitchen staff).

On 2021-10-15 23:10:46, user Steve wrote:

I agree this study should be final at this point but I'm not sure the peer review process is even a real thing anymore. Maybe I am too cynical but I find it striking that we can spend almost two months debating about why this study wasn't perfect (either way) yet nobody seems able or interested in putting together a better study to address a simple question: How long does natural immunity last? We have tons of stats on who got covid, and what percentage of people are vaxxed but we can't seem to find any of those recovered patients and test them today for antibodies? <br /> The CDC just released their "study" of a few hundred people in Kentucky that they say proves vaccination is better. Hard to take them seriously when a real study involving almost 50,000 patients is dismissed because it isn't perfect.

On 2021-08-29 01:52:08, user bubba gump wrote:

Yes, I don't believe this can possibly be accepted for publication without addressing the glaring errors and overlooked biases. It's a shame that the antivaxxers are already trumpeting this as vindication for their wrong choices.

On 2021-09-05 04:24:28, user Adriana Perez wrote:

Regrettable the matching of the groups requires to use conditional logistic regression for the analysis which the authors did not do otherwise they would have written it. The lack of control in the matching indicates that the results can not be trusted.

On 2022-01-06 02:01:18, user Stoichastic wrote:

"What makes you think that mutations on the nucleocapsid are anymore stable than the mutations on the spike protein"

Stability is a function of mutation and selection pressure, not degree of freedom to mutate. There's no selection pressure on the nucleocapsid, effectively, just the spike.

You only need to check out VOC mutation info to see the spike is changing significantly more than nucleocapsid thanks to the vaccines.

On 2021-08-26 04:22:25, user brisalta wrote:

The paper does not clearly state which variant the subjects were previously infected with. If that data is available it may be useful to include that information.

On 2021-09-02 18:28:43, user Kostas Damdas wrote:

Who were the participants? people vaccinated in january vs people covid positive recently? immunocompromised vs healthy?

On 2021-01-10 19:47:40, user Wayne Griff wrote:

21 days after the 1st dose of the Pfizer Vaccine, patients have 1/5th the viral neutralizing power of Convalescent Plasma. In contrast, 7 days after the 2nd dose, patients have 2-4 times the neutralizing power of Convalescent Plasma. NEJM Also, the 47% effectiveness rate is only up to 3 weeks. It's definitely going to be less at 6, 9, or 12 weeks.<br /> Giving only 1 vaccination is a waste of a vaccination. It provides little, if any immunity.

On 2020-04-29 17:12:43, user Deirdre wrote:

It isn't clear whether you are aiming to predict mortality or identify causal risk factors. There is a difference, they have distinct approaches. The title for the final figure is confusing, instead of "Survival by symptom onset", do you mean "Risk of mortality"? There are limitations in BMI as a proxy for total fat mass in elderly populations that may be underestimating the relationship of obesity, and is a notable limitation.

On 2020-05-14 10:44:33, user Dom Mcelhinney wrote:

In the at risk group for covid19 almost 50% of population are being treated for Hypertension and Hypercholesterolaemia. Can you explain why you have been unable to list this as a possible comorbidity.

On 2021-01-29 12:29:23, user stephan walrand wrote:

Nice correlation with the cloudiness and sun light insolation, but which is also compatible with vitamin D production!!! However, it is obvious that when comparing deaths from March to July, it is impossible to see any latitude correlation, because sun elevation averaged between March-July is almost equal for all countries.

On 2020-04-16 01:21:40, user Bobenheimer wrote:

No more updates of the projections? Data tracking stops on 4/12.

On 2021-06-11 13:44:12, user Jay Alan Erdman wrote:

Where to begin? 1) This is an abstract; not yet peer reviewed; so it's just four guys saying this. 2)They don't say how they got their population. 3) They provide no data. 4) There is no control group either randomized, case control, or cohort. 5) They really do not specify their methods. 6) There is no treatment protocol so we don't know what additional treatment they may have received. Overall this doesn't meet any scientific standard. But even if it had been well done; these patients presented in the Spring of 2020 when treatment protocols were very different and outcomes much worse. This study says nothing about whether HCQ would be of any benefit to patients receiving treatment in Spring 2021.

On 2021-09-02 22:59:18, user Alberto wrote:

One of the 2 positives in the experimental group was on day 2 after randomization, which means that this was almost surely a pre-infection. Then the second one is on day 5, just like the first one in the control group. Day 5 is dubious (whether it can be considered a pre-infection or not). After day 5, it was 0 positives in the experimental group vs. 9 positives in the control group. That's very significant even with the low numbers. Counting day 5 as valid, it's 1 vs. 10. Still very significant.

On 2020-03-30 04:18:55, user Joe Carano wrote:

North Africa spread started in mid February, and might have even started earlier in Egypt. So, no it's not late in the line. It's concomitant.

On 2020-04-11 07:32:16, user adss wrote:

Injecting BCG is basically injecting controlled and weakened viruses, so that your body can create the anti-body. Usually people that have weak immune systems need to be careful not to catch the disease from the vaccine.

On 2020-04-08 07:30:20, user Lara wrote:

It does not appear that the authors adjusted for number of tests conducted. There is a significant difference in the number of tests conducted in high income like the US (>2 million) versus LMIC like South Africa (1700 tests). Right now it can't be assumed that BCG is protective, when the full scope of the problem is not unknown, or in other words true case load is presented.

On 2020-04-01 18:41:26, user Ronald McCoy wrote:

This totally glosses over China. Huge case numbers with universal BCG vaccination. This is a classic example fo confirmation bias. This article has more holes than a Swiss cheese factory.

On 2020-06-06 13:55:03, user Jürgen Heuser wrote:

Thx very much for this very helpful work!!

I'm afraid I do not understand the term <br /> "Comorbidities marked by * are defined by hospital discharge diagnoses in combination with drug redemptions (i.e. filled prescription within 6 months prior to the test date. Of note, there is a lag of 15 days on prescription data)" <br /> when applied to diagnoses like alcohol abuse, overweight or dementia. What kind of medication prescribed would qualify a patient into those categories?

Best <br /> Jürgen Heuser

On 2021-09-23 06:52:46, user White Rabbit wrote:

There are several issues about the meta-analysis by Martinoli et al. for example they wrote they did a meta-regression in order to explain the the huge between-study heterogeneity affecting the results, but no meta-regression results appears anywhere. They observed a statistically significant publicaton bias ("We found an indication for publication bias (P=0.03)" ,page 10) a serious but unaddressed issue. Ther are also inconsistencies between the results and the conclusions, e.g. though they found that "Children and adults showed comparable SARS-CoV-2 positivity <br /> rates in most studies" (page 9)" the abstract reads "children are 43% less susceptible than adults".Furthermore in some tables and forest plots, they used as denominator the total of students and staff altogether instead of students only, to estimate the students incidence.

On 2020-04-16 22:12:24, user Amy E. Herr wrote:

During the COVID-19 pandemic, we are grateful for the authors’ urgency in assessing N95 respirator decontamination methods. It is in this spirit of collegiality that we draw attention to an aspect that could (unintentionally) cause confusion: the PS19Q thermopile sensor mentioned in the Methods section does not appear to be suited to detect the virus-killing UV-C light emitted from the source. The authors are aware of the possible confusion and are working diligently to check into and, if needed, address the concern.

As background: from the manufacturer’s specifications, the PS19Q thermopile sensor mentioned in the preprint appears to only detect wavelengths as low as 300 nm, which is above the UV-C germicidal wavelength range (<280 nm). Low-pressure mercury UVGI bulbs emit a 253.7 nm peak [EPA]. 260 nm is the peak UV-C germicidal wavelength for inactivating virus via DNA and RNA damage [Kowalski et al., 2009, Ito and Ito, 1986]. The germicidal efficacy arises primarily from the UV-C dose, with the UV-B dose (280-320 nm) providing significantly lower germicidal efficacy. At 300 nm, UV light is ~10x less effective at killing pathogens than at 254 nm [Lytle and Sagripanti 2005]. UV-A dose (320-400 nm) is considered minimally germicidal [Kowalski et al., 2009; Lytle and Sagripanti 2005; EPA]. We are concerned about the potential adverse health outcomes that might stem from use of the PS19Q thermopile sensor not matched to the UVGI wavelengths for N95 FFR decontamination.

As best practices, all researchers working on UV-C methods are encouraged to use a calibrated, NIST-traceable, UV-C-specific radiometer to report not just UV-C irradiance, but also UV-C specific dose, as a minimally acceptable UV-C dose of 1.0 J/cm^2 is sought on all N95 FFR surfaces. For additional detail from the peer-reviewed literature, please see the 2020 scientific consensus summaries on N95 FFR decontamination at: n95decon.org

Again, we thank the authors for their timely research and quick action to confirm suitability of their experimental design, all of which aim to better inform decision makers working to protect the health of heroic front-line healthcare professionals during the COVID-19 pandemic.

References cited: <br /> • Manufacturer’s specifications, the PS19Q thermopile sensor: https://www.coherent.com/me...<br /> • EPA: ULTRAVIOLET DISINFECTION GUIDANCE MANUAL FOR THE FINAL LONG TERM 2 ENHANCED SURFACE WATER TREATMENT RULE: https://nepis.epa.gov/Exe/Z...<br /> • Kowalski et al., 2009: https://link.springer.com/c...<br /> • Ito and Ito, 1986: https://onlinelibrary.wiley...<br /> • Lytle and Sagripanti 2005: https://www.ncbi.nlm.nih.go...

On 2020-08-03 13:54:21, user Charles R. Twardy wrote:

Forgive me if this is covered in the paper - today I am just skimming abstracts. But another preprint out today shows a mortality risk reduction of 0.7 per 100 kJ/m^2 of ultraviolet (UVA) exposure, in three countries measured at the county level. Is US altitude a proxy for UVA? Vice versa? Could you two combine models to look for residual effects?

On 2021-12-01 23:56:02, user Athanasios Chalkias wrote:

The article has been published in Clinical Hemorhelogy and Microcirculation and can be found here: https://content.iospress.co...

On 2021-10-27 07:45:56, user Andy Bloch wrote:

No, you did not read a study that suggested a drop in effectiveness of 40% every 30 days. Maybe you read a study that suggested a drop in antibody levels that large, but there isn't a linear relationship between antibody levels and vaccine effectiveness.

On 2021-09-11 13:25:33, user J Jones wrote:

What you clearly dont understated is that the injection DOESNT PREVENT YOU FROM CONTRACTING COVID OR FROM SPREADING IT. Where is this misinformayion coming from?

On 2020-04-22 04:36:02, user Paul Hue wrote:

Has Covid19 been truly isolated? Have its purported surface proteins been linked to genetic sequences in recovered genetic material from a true isolation?

On 2020-04-18 08:24:25, user YishaiK wrote:

I am sorry to say that the basic assumptions and math of this research are wrong.<br /> The researchers quoted the kit performance provided by the manufactures, but quoted the wrong information, twice.<br /> The correct information appears here: http://en.biotests.com.cn/n...

A short introduction: Estimating the real prevalence from the sampled one depends on the accuracy of the serology kit used. The lower the sensitivity of the kit, the higher the estimate should be in comparison to the survey results. On the other hand, the lower the specificity of the kit, the lower the estimate should be.

Now we're ready to explain how the researchers got it all wrong:

Since the decision of being positive for covid-19 was taken by IgG *or* IgM,<br /> then the kit sensitivity should be taken as the unity of both IgG and IgM, which leads to 100% sensitivity, and not 91.8% as taken in the research (the writers "chose" to quote the lower sensitivity relating to IgM only, which is just wrong).

It gets worse - when quoting the specificity of the kit, the writers quoted the higher level of 99.5% which fits this time to IgG only (how convenient). But again, since the criteria in the survey was IgG *or* IgM, the specifity is actually lower - at maximun 99.1%, and possibly even 98.65% (if the false-positives in the manufactures validation were for different people between IgG and IgM).

Taking both these mistakes into account (i.e. assuming 100% sensitivity and 98.65% specificity) - the estimated prevalence (before correcting by sex age etc., which I find to be irrelevant) is a mere 0.15%. A lot less exciting.

I find it surprising that the writers quoted different (let alone wrong) values for sensitivity and specificity (once IgM and once IgG), in a way that miraculously led to higher prevalence estimations.

I allow myself to ignore the writers self validation of the kit, since specificty was tested accross an outrageously small sample size of 30 non- Covid19 samples. As the writers acknowledged themselves, that is only enough to ensure the kit has a specificity above 90%. Nothing to write home about.

To sum it up, the research found 50 positives out of 3,330. This can teach us more about he false-positive of the serology kit used, than about the real prevalence of Covid-19 in the population surveyed.

There are lies, and then there are statistics...

On 2020-04-18 13:42:31, user martingugino wrote:

If every inhabitant of New York City (other than those who fled) has antibodies, the new infection rate would have to be zero. Correct?

On 2020-04-17 21:28:07, user Daniel Shanklin wrote:

This study abstract should be rewritten as follow: "A study of Facebook users who thought they might have COVID-19 resulted in a roughly 2.49% to 4.16% positive-test rate"

The fact that you've extrapolated this to an entire population is confounding.

On 2020-04-18 15:49:32, user DickRuble wrote:

There are many question marks about this study re: population sampling and analysis.

I could find no info about the manufacturer of the test. Could it be that the test/antibody is not specific enough, and detects exposure to other coronaviruses, such as the common cold? I.e. many false positives?

On 2020-04-19 21:23:49, user figureitout1 wrote:

I am not in the field and have no expertise but I think this study may have measured just the prevalence of the common cold in Santa Clara county. The ELISA assays for IgG and/or IgM antibodies are known to give false-positives due to the other Corona viruses that give us the common cold. It is known from European studies that the common cold in the winter time can cause roughly 3% positive Covid-19 ELISA tests – just about what was measured in this study. In order to get meaningful results a second test (neutralization test that is not sensitive to the common cold viruses) needed to be done on the positive samples. The scientifically correct conclusion of the study would be: the Covid-19 prevalence is between 0% and 4%. It seems irresponsible to put the study on the web and have people, including politicians, jump to hasty and possibly wrong conclusions.

On 2020-04-22 03:00:50, user Eric Hadley-Ives wrote:

I think there has been a correction on that other paper that the test getting 87% was not the same test (it was the same manufacturer) as the one used by the Stanford Sample. An earlier version of that paper did not point out this.

On 2020-04-18 18:54:22, user Tomas Hull wrote:

Germany had a similar study done published on April 9, where they combined the antibody test with the polymerase chain reaction test in active infections.

Nature reviewed both this study, and the one from Germany, where the combined results in a population of a town of 12,000 revealed overall 15% infection rate.

https://www.nature.com/arti...

On 2020-04-19 17:20:25, user James Kalb wrote:

Does anyone know which antibody test was used in this study? Maybe I overlooked it. I’m interested in the name of the manufacturer.

On 2025-10-14 23:19:52, user T. De La Cruz wrote:

On behalf of the authors, we would like to update to the medRxiv community that the present preprint is now published in a journal and available at https://doi.org/10.1016/j.ijidoh.2025.100078 .

On 2021-08-31 01:53:43, user William Brooks wrote:

The results of the proposed model rely on three questionable assumptions: 1) masks are effective at preventing infection [1]; 2) infection risk decreases as mask usage increases [2]; and 3) masks are more effective than ventilation [3].

However, the authors ignore real-world data challenging these assumptions even though they reference the UK's Events Research Programme (ERP), which found little difference between Phase 1 events with and without mask requirements [4]. Moreover, recent ERP data for large-scale sporting events without mask requirements "demonstrate that mass participation events can be conducted safely, with case numbers comparable to, or lower than community prevalence" [5].

In short, the authors should base their models on real-world data rather than unproven assumptions.

[1] https://www.acpjournals.org...<br /> [2] https://escipub.com/irjph-2...<br /> [3] https://aip.scitation.org/d...<br /> [4] https://www.gov.uk/governme...<br /> [5] https://www.gov.uk/governme...

On 2020-04-15 18:32:13, user Jaime Navarro wrote:

There is a significant flaw in this paper's claim that Type A blood types are more susceptible to CoViD-19, and type O are less. In that the paper does not address the susceptibility of those with type B or AB blood. If as the paper suggests type O blood sees the virus as a type A antigen and so attacks the virus. Shouldn't the same happen in patients with Type B or AB? After all they would have antibodies to type A the same as type O people would.

On 2020-04-02 15:02:30, user Quaid wrote:

I would love to know if there is a difference between O positive and O negative. Have you gotten a response?

On 2020-05-15 23:52:54, user Milesy Mathis wrote:

At least they included Zinc. That's progress.

On 2020-07-09 20:12:01, user scott kelley wrote:

Where is the trial with immediate treatment at time of positive test in patients over 65 without ekg abnormalities. Like all antivirals, early treatment is the key.

On 2021-10-26 17:04:29, user Robert wrote:

In the history of Vaccines I have yet to see where a drug company is not working on a new or altered vaccine within 6 months of the original. Given the speed these vaccines were released you would think that alternate or new and improved mRNA would be released or spoken of. I have seen nothing or read nothing. <br /> Additionally. This is the only vaccine I ever seen pushed that does not have the listed side affects.

On 2020-04-19 16:05:15, user jmacon wrote:

Sweden: deaths per 1M = 152, Switzerland: deaths per 1M = 160. Sweden does have fewer deaths than Switzerland. We all need to be careful with our facts. Yes, the rate is lower in Denmark and Finland. But Sweden is much better than most of the European Union countries. No lockdown whatsoever and certainly no explosion. Actually results most countries would be very happy about.

On 2020-04-19 15:53:35, user JGaltbna wrote:

Nothing happens “right now”. I suggest actually reading the WH plan to reopen and what has to happen before anything is “relaxed” per policy. 3 phases, each lasting at least 14 days? Ring a bell? The only restrictions being eased now are things that should never have been restricted like walking on a beach. The danger isn’t the policy but that people ignore the policy.

On 2021-08-07 16:28:29, user k wistar wrote:

I am wondering how you looked at this particular set of data and came to that particular conclusion. Can you walk us through your analysis of the data?

On 2021-10-27 17:47:28, user Sir Henry wrote:

The definition of "Severe COVID-19" did not require hospitalization and was therefore in most cases not life threatening. COVID-19 frequencies cluster at the mild end of the disease. Connecting worst-case possibilities from the definition to mortality is a red herring, because there was no mortality signal.

HR > 125 plus fatigue and a positive lab test would have qualified as "severe COVID-19" under the study definition. That seems very similar in severity to debilitating fever.

On 2021-08-11 12:11:31, user Truenorth 1960 wrote:

I'm not sure I understand this study. While I understand this is a report that is intended for professionals, the l language is not English, it is "technobable" for lack of a better expression. For covid , these studies should have a translation into something more akin to regular English. Narrative should help understand the results. In this case I find the narrative is not helpful, it is easier to look at the tables.

On 2021-09-18 19:05:19, user OBS wrote:

These long-term results from Pfizer's clinical trial are quite informative- does anyone know of a corresponding preprint from Moderna containing their long-term (i.e. 6 months or so) clinical trial results, particularly regarding safety (total deaths, adverse events, etc.) Moderna has said it's efficacy at 6 months was 93% (a tiny bit better than Pfizer), and all 3 COVID deaths by 6 months were in the placebo group (also better than Pfizer's result of 1 COVID death with vaccine vs. 2 COVID deaths with placebo). This is not at all surprising considering that Moderna's vaccine dose is over 3x higher than Pfizer's. But what about Moderna's results for total deaths, how do they compare to Pfizer's? Surely, so many people here would like to know.

The following is stated in an article from 3 days ago on Moderna's website:

"Additionally, the Company shared a new analysis of follow-up through 1 year in the Phase 3 COVE study suggesting a lower risk of breakthrough infection in participants vaccinated more recently (median 8 months after first dose) compared to participants vaccinated last year (median 13 months after first dose). Manuscripts summarizing both findings have been posted to preprint servers and will be submitted for peer-reviewed publication."

However, no such preprint from the COVE study seems to show up- does anyone know how to find it?

On 2021-08-04 12:33:07, user Will Helm wrote:

the 14+15 deaths are not vaccine related, bur are "normal demographic" deaths.<br /> A study of Pfizer for European nations based on Eudravigilance values gives a ratio of 15 vax-related deaths per million doses. We can assume it's the same thing for this study. So, for 22'000 who received the shots, statistically there's no death possible due to the jab.

On 2021-08-05 16:37:19, user circleofmamas wrote:

So by not being vaccinated, I am reducing my relative risk of a 'severe adverse event' by 74%. And my absolute risk to become a "case" is less than 4%, and severe COVID is 0.1%.

On 2025-11-30 16:56:07, user Cyril Burke wrote:

RESPONSE TO REVIEWER #1

June 27, 2022<br /> Re: Longitudinal changes in creatinine signal early decline in glomerular filtration rate without consideration of age, sex, ‘race’, and nationality

We greatly appreciate that the reviewers were thorough, fair, and helpful in their comments.

Comments to the Author

Reviewer #1: Burke et al submit a somewhat unusual paper, devoted to a topic of potential major clinical relevance, and as yet understudied.

General comments

1. The thesis of the authors, that using the baseline serum creatinine of a given patient would potentially improve the earlier diagnosis of kidney disease, even in the normal range, is in line with the experience of this reviewer, who always retrieves, whatever the difficulty of reaching that goal, past results of blood tests, and uses them as a way to date the onset of kidney disease, sometimes with important prognostic implications.

Your experience adds support to the literature suggesting that historical sCr levels provide a context for sCr changes. These benefits might encourage investments in digital data exchanges so that electronic health records (EHRs) can ease collection and presentation of sCr results from multiple commercial and hospital laboratories.

2. Yet, the authors do not provide data strongly supporting their thesis. For instance, when looking at case 2 [now Patient 3], should the last point (the most recent one) be omitted, there would be very little evidence supporting progressive early kidney disease.

We advocate prospective monitoring of longitudinal sCr as a proxy for glomerular filtration rate (GFR). The Cases were meant to show that charting the data and simple follow-up over several visits and months can allow general clinicians to differentiate CKD from other explanations for increased sCr. The four case histories represent patients in a non-nephrology medical practice with borderline eGFR that raised the possibility of CKD. In each of these cases, retrospective collection of sCr values suggested varied explanations for the elevated sCr, and we expect many cases will represent sCr influences other than CKD, not necessarily warranting nephrology referral. Armed with this tool, and used prospectively, Physicians, nurse practitioner, and physician assistants (PCPs) might identify and manage the 90% of patients with currently unrecognized CKD.

3. The claim that the statistics fit the data better when all points are used (page 9,11) should not come as a surprise. Using thresholds instead of the full range of values has long been known to be more powerful for statistical analysis. But fitting the data does not equal to a high positive predictive value!

We agree that this is counterintuitive, so we thought this was an important point to discuss. Research methods that get translated into clinical settings rely on assumptions that are not always familiar to healthcare workers. Whatever the merits of thresholding conventions, understanding their mathematical underpinnings can inform a more nuanced interpretation of lab results. The revision includes our initial, intuitive assessment of the data and the interpretation of the residuals – from a mathematics perspective. Lack of awareness about residuals can easily lead to improper interpretation of thresholded lab data. The use of statistics is not intended to document superiority of fit but rather to demonstrate how simplifications with practical clinical value may gloss over clinically relevant information in some cases. The inclusion of additional charts seeks to take it away from abstracted statistics and toward more intuitive clinical concerns. We favor early diagnosis of kidney injury through investigation of nonspecific changes in longitudinal sCr. This method seems usable and may be manageable by PCPs using a time frame of several visits over several months to separate false positives, which may be influenced by chance attributable to the mathematical properties of lab data.

4. A key question is whether in a real-world context, the earlier diagnosis of kidney disease would be possible, without too much background noise from intercurrent illness (functional), drugs (NSAIDS, etc.). In other words, would the specificity (or PPV) of the suspicion of early kidney disease be reasonable enough to catch the attention of clinicians

We think so. We believe longitudinal serum creatinine (sCr) will encourage dialogue between patients and clinicians, raising awareness of the importance of avoiding kidney injuries that often happen out of sight and out of mind until, for far too many, culminating in urgent dialysis. In the same way that patients now ask for their blood pressure, we anticipate patients tracking their own sCr and kidney risks. Decades after introduction of the mercury sphygmomanometer, PCPs learned how to manage blood pressure to improve health. We believe longitudinal sCr can soon be a widely used tool because the concepts are old, there is a broad literature supporting this approach, and the value can be enhanced by more frequent testing of sCr. This is what PCPs do – sort the random cough, costochondritis, or stress response from nascent pneumonia, angina, and hypertension. PCPs already worry about the kidneys. They may welcome a tool to accompany the chest radiograph, electrocardiogram, and sphygmomanometer.

Of interest, the decision analysis by den Hartog et al found markedly more false-positive diagnoses of CKD with eGFR than with serum creatinine alone.

5. Even though there has been improvement in the standardization of measurement of serum creatinine (IDMS), the comparability of results measured by different labs remains suboptimal, at least in the experience of this reviewer, and medical shopping is not uncommon, making the availability of all previous results in the same graph a logistical challenge.

We share this concern, which laboratorians have wrestled with for many years and will not be solved soon. However, we propose utilizing the maximum serum creatinine (sCr-max) to smooth the variability of these inputs (as well as the variability from patient diet and hydration). One laboratory will be the highest, and when patients use multiple laboratories, one laboratory may more often define the sCr-max. As patients learn the rationale for using the same lab, we believe most (not all) will voluntarily use one or perhaps two labs (as they mostly do when we repeating longitudinal MRI imaging studies, for example). The sCr-max reduces the effect of variability between laboratories, allowing clinical insights even without future improvements in sCr assays.

Australia, Canada, and the United Kingdom have stricter sCr analytical performance goals than the United States, which could improve its sCr comparability by matching their standards.

Specific comments

1. The authors should mention that the USPTFS decided a month ago to revisit the question of screening for kidney disease in high-risk groups (page …)

One reference stated that this initiative has not been announced publicly but is “under active consideration” by USPTFS because “…for a screening to help people live longer, healthier lives, clinicians must be able to treat the condition once it is found. The existence of effective treatments is one of many important factors that the Task Force considers.” This perspective is surprising because it ignores the potential of effective prevention by avoiding NSAIDs, hypotension, dehydration, and nephrotoxic medical treatments (e.g., aminoglycosides). We, too, look forward to updated findings from USPTFS.

2. Even though ESRD has a legal meaning in the USA, not very relevant to the topic of this paper about early kidney disease, the authors should stick to the nomenclature proposed by a recent KDIGO consensus conference (see Levey et al. Nature Reviews in Nephrology). In particular, use kidney failure instead of ESRD/ESKD. When the topic is glomerular filtration, use that wording instead of kidney function (page…)

We have adopted this terminology and would welcome any further recommendations.

3. The authors allude to the concepts of prediabetes and prehypertension. But this reviewer points to the fact that the levels used to define those entities are currently “generic”, rather than based on previous values in an individual subject. Please discuss.

We understand that the normal population ranges for serum glucose and blood pressure are narrower, with less interindividual variation, so population reference ranges work well for monitoring diabetes mellitus and hypertension. Unfortunately, this is not true for serum creatinine, though within-individual reference of longitudinal sCr appears to facilitate diagnosis of pre-CKD.

4. The authors repeatedly mention in the discussion section evidence that even small increases in serum creatinine have prognostic significance. This has indeed been known for decades but is a different topic: AKI. Admittedly, there is growing evidence that AKI and CKD are linked. But that the stability of a biological parameter is prognostically best is all except surprising: the same is true for body weight, mood, blood pressure etc.

We agree that AKI and CKD appear to be merging and this may become clearer from more frequent sampling and charting of longitudinal sCr. What has been missing is graphical representation of the data to allow quick assessment for CKD in long-term trends, and this may soon be obtainable from EHRs and IT departments, which should end the practice of deleting historical data of value to longitudinal analysis.

[See next comment for Response to Reviewer #2.]

On 2025-11-30 16:49:17, user Cyril Burke wrote:

[Note: This is the first of several reviews of an earlier version of our combined manuscript that aims to reduce ‘racial’ disparity in kidney disease. The comments were kindly offered by nephrologists, through a medical journal, and we remain grateful to them for the time and care they gave to improve our manuscript.

We removed identifying features and will include our responses in a subsequent comment. The changing title and line numbers refer to versions prior to our medRxiv preprints.]

April 1, 2022<br /> Screening for early kidney disease and population health using longitudinal serum creatinine

Dear Dr. Burke III,

REDACTED.

Reviewer #1: Burke et al submit a somewhat unusual paper, devoted to a topic of potential major clinical relevance, and as yet understudied.

General comments

1. The thesis of the authors, that using the baseline serum creatinine of a given patient would potentially improve the earlier diagnosis of kidney disease, even in the normal range, is in line with the experience of this reviewer, who always retrieves , whatever the difficulty of reaching that goal, past results of blood tests, and uses them as a way to date the onset of kidney disease, sometimes with important prognostic implications.

2. Yet, the authors do not provide data strongly supporting their thesis. For instance, when looking at case 2, should the last point (the most recent one) be omitted, there would be very little evidence supporting progressive early kidney disease.

3. The claim that the statistics fit the data better when all points are used (page 9,11) should not come as a surprise. Using thresholds instead of the full range of values has long been known to be more powerful for statistical analysis. But fitting the data does not equal to a high positive predictive value!

4. A key question is whether in a real world context, the earlier diagnosis of kidney disease would be possible, without too much background noise from intercurrent illness (functional), drugs (NSAIDS, etc..). In other words, would the specificity (or PPV) of the suspicion of early kidney disease be reasonable enough to catch the attention of clinicians

5. Even though there has been improvement in the standardization of measurement of serum creatinine (IDMS), the comparability of results measured by different labs remains suboptimal, at least in the experience of this reviewer, and medical shopping is not uncommon, making the availability of all previous results in the same graph a logistical challenge.

Specific comments

1. The authors should mention that the USPTFS decided a month ago to revisit the question of screening for kidney disease in high risk groups (page …)

2. Even though ESRD has a legal meaning in the USA, not very relevant to the topic of this paper about early kidney disease, the authors should stick to the nomenclature proposed by a recent KDIGO consensus conference (see Levey et al. Nature Reviews in Nephrology ). In particular, use kidney failure instead of ESRD/ESKD. When the topic is glomerular filtration, use that wording instead of kidney function (page…)

3. The authors allude to the concepts of prediabetes and prehypertension. But this reviewer points to the fact that the levels used to define those entities are currently “generic” , rather than based on previous values in an individual subject. Please discuss.

4. The authors repeatedly mention in the discussion section evidence that even small increases in serum creatinine have prognostic significance. This has indeed been known for decades but is a different topic: AKI . Admittedly, there is growing evidence that AKI and CKD are linked. But that the stability of a biological parameter is prognostically best is all except surprising: the same is true for body weight, mood, blood pressure etc…

Reviewer #2: Thank-you for the opportunity to review this work which highlights the importance of monitoring serum creatinine over time and how this can be a useful tool in detecting possible CKD. This is an important topic as the use of sCr on its own is certainly under-utilised and changes are often missed because they don’t fall into a predefined category.

MAJOR CONCERNS

“Choi- rates of ESRD in Black and White Veterans” doesn’t fit with the rest of the paper including the title; the introduction and conclusion also don’t adequately address this portion of the paper. It feels disjointed from the main point of discussion which is the use of sCr in screening “pre-CKD”. This section and discussion should be removed and possibly considered for another type of publication.

Cases 1 - 3, (lines 93 – 122): where are these cases from? There is no mention of ethics to publish these patient results, which appears to be a clear ethics violation. If so, these cases should be removed and patient consent and ethical approval obtained to publish them.<br /> The authors describe the reasons for not obtaining an ethics waiver for this secondary data analysis. Despite this, the relative ease of obtaining an ethics waiver for secondary data analysis usually means that this is done regardless.

The message of the article and data representation is unclear: do the authors wish to show that sCr is superior to eGFR in this “pre-CKD” stage, should both be used together? Do the authors wish to convey that a “creatinine blind range” does not exist? Or is the aim to demonstrate that continuous variables should not be interpreted in a categorical manner?

MINOR CONCERNS

ABSTRACT<br /> Vague<br /> Doesn’t give a clear picture of the study

INTRODUCTION<br /> 51 – 57: needs to state that these stats are from e.g. the US. The authors should consider adding international statistics to complement those from the US.

68: reference KDIGO guidelines, state year

75 – 77: is this reference of the New York Times the most appropriate?

82: within-individual variation not changes (this is repetition of the point made in lines 425 – 427, but should match the language)

82 – 84: reference? If this is a question it should be presented as such

84: “normal GFR above 60” = guidelines (including KDIGO) do not refer to 60 as normal GFR, 60 – 89 is mildly decreased. (see line 126)

93: avoid the use of emotive words such as apparently (also in line 428)

94: “Not meeting KDIGO guidelines”: KDIGO 2.1.3 includes a drop in category (including those with GFR >90). This would appear to include some of the cases listed. Additionally, albuminuria should have been measured for case 2 and 3.

97: “progressive loss of nephrons equivalent to one kidney”: this is based on a single creatinine measurement.

93 – 122: Could any of these shifts be explained by changes in creatinine methodology or standardisation of assays, especially over 15 – 20 years (major differences between assays existed before standardisation and arguably still exist with certain methods).<br /> It would be useful to see a comparison between serial sCr and eGFR measurements on the same figure. There appears to be significant (possibly more pronounced) changes when eGFR is used. As line 87 mentions changes in eGFR may be as useful (and in some situations more useful) than changes in sCr alone.

127 – 142: should there be separate charts for males and females, the differences in creatinine between males and females needs to be discussed somewhere in the paper. Similarly, is this suitable for all ages?

162 – 163: rephrase

METHODS<br /> 185 – 193: aim belongs in the introduction, can be adjusted to complement paragraph 178 – 182.

196 – 205: reference sources

224 – 247: not in keeping with the rest of the article or title and conclusion

RESULTS<br /> If eGFR is treated as a continuous variable does inverted sCr still have higher accuracy?

As mentioned, the section on ESRD in black and white veterans doesn’t fit in with the rest of the article.

DISCUSSION<br /> As mentioned, section 4.1 doesn’t fit in with the rest of the article. As the authors note the correlation between illiteracy and CKD is likely not causal.

387: erroneous creatinine blind range. The data presented does not show this is erroneous there is still a relative blind range. A distinction must be made between a population level “blind range” and an individual patient’s serial results. The data and figure 4 in particular demonstrate the lack of predictive ability of sCr above 40ml/min compared to below 40ml/min at a population level. For an individual patient this “blind range” is more relative, and a change in sCr even within the normal range may be predictive. (Note: the terminology “blind range” is problematic).

399 – 400: “rose slowly at first and then more rapidly as mGFR decreased below 60” this refers to a relative blind range. Whether these slow initial changes can be distinguished from analytical and intra-individual variation is the question that needs to be answered before we can say a “blind-range” doesn’t exist for an individual patient.

425 - 432: sCr is indeed very useful when baseline measurements are available. eGFR remains useful when baseline sCr is not available or when large intervals between measurements are found.

425: low analytical variation- if enzymatic methods are used

428: avoid the use of “apparently”

430: reference 56 compares sCr and sCysC with creatinine clearance NOT with mGFR, this does not prove that mGFR has greater physiologic variability. Creatinine clearance is known to be highly variable (partially due to two sources of variability in the measurements of creatinine: serum and urine).

The limitations of sCr for screening should also be discussed: differences in performance and acceptability between enzymatic and Jaffe methods (still widely used in certain parts of the world), the effect of standardizing creatinine assays (an important initiative but one that could also produce shifts in results around the time of standardization- see cases), low InIx means that once-off values are exceedingly difficult to interpret, is a single raised creatinine value predictive (or should there be evidence of chronicity): similarly are there effects from protein rich meals, etc (The influence of a cooked-meat meal on estimated glomerular filtration rate. Annals of Clinical Biochemistry. 2007;44(1):35-42. doi:10.1258/000456307779595995)

CONCLUSION<br /> The discussion recommends using SCr above eGFR while the conclusion recommends the NKF-ASN eGFR for use in pre-CKD and ASC charts. While the use of both together in a complementary fashion is understandable- this needs to be congruent with the discussion, aims and results.

On 2020-05-18 21:11:52, user MG wrote:

Don't forget the time period of data collection was the Dec-Feb time frame (case reports dated 1/4/2020-2/11/2020). Most of China is cold then; there just weren't many people spending time outside during that time period.

On 2020-05-19 00:53:07, user Sinai Immunol Review Project wrote:

Main Findings:

An unusually high incidence of Kawasaki disease was reported in a pediatric center for infectious diseases in France. This is a rare post-viral vasculitis that was been associated with several viruses in the past, including coronaviruses. The authors reported 17 cases over a period of 11 days, in contrast to a mean of 1 case per 2-week period in 2018-2019. <br /> Polymorphous skin rash and bulbar conjunctival injection were the most frequent criteria for diagnosis of Kawasaki disease. The patients had a median age of 7.5 years (range 3-16); 65% (n=11) presented with shock syndrome, and 70% of the patients (n=12) had concomitant myocarditis. All patients had high inflammatory parameters, including leukocytosis with a predominance of neutrophils, and high levels of C-reactive protein, procalcitonin and interleukin-6. Compared to past descriptions of Kawasaki disease, this cohort had an 8-fold increase in procalcitonin level, what suggests a particularly strong post-viral immunological reaction to SARS-CoV-2 as compared with other viral agents. <br /> Remarkably, although the study was conducted in France, 59% of the patients were originally from sub-Saharan Africa or Caribbean islands, and 12% from Asia, pinpointing a possible genetic predisposition or a travel-associated exposure. <br /> In 82% of the cases, IgG antibodies for SARS-CoV-2 were detected, suggestion an association with coronavirus disesase 2019 (COVID-19). RT-PCR testing for SARS-CoV-2 was positive in 41% of the patients. Although only 6 patients had recent history of an acute respiratory infection, in 9 cases there was history of recent contact with family members displaying respiratory symptoms. However, all patients had gastrointestinal symptoms prior to the onset of Kawasaki disease signs.<br /> All patients were treated with intravenous immunoglobulin (IVIG) and aspirin. Some received concomitant corticosteroids (n=3) and/or broad-spectrum antibiotics (n=14). Admission to intensive care unit (ICU) was necessary in 13 cases. A total of 5 patients had IVIG resistance. Regarding the outcome, 5 patients had not yet been discharged by the time the manuscript was published.

Limitations:

This was a single-center study with a very short follow-up period of 11 days. The information about the total number of paediatric patients that tested positive for SARS-CoV-2 in this center/region during the reported period is missing. That could help to draw conclusions about the incidence of Kawasaki disease-like inflammatory syndromes in children after SARS-CoV-2 infection. Additional to the genetic predisposition hypothesis, information about potential travel-associated exposures should be discussed in the manuscript due to the apparent difference in incidence between racial groups. Furthermore, although the prevalence of COVID-19 in Europe is currently very high, an association between SARS-CoV-2 and the reported outbreak of Kawasaki disease needs further studies to determine causality.

Significance:

The temporal association between the COVID-19 pandemic and the results of RT-PCR and antibody testing suggest a causal link between Kawasaki disease and COVID-19. At the time of this writing, while this is not the first description of Kawasaki disease-like inflammatory syndromes in association with COVID-19, it is the largest published cohort. Kawasaki disease should be evaluated as part of the spectrum of post-viral immunological reactions in COVID-19 convalescent children. These findings should prompt a high degree of vigilance among all physicians, and preparedness in countries with a high proportion of children of African and Asian ancestry during the COVID-19 pandemic. The World Health Organization (WHO) has recently developed a case report form and encouraged physicians to report all suspected cases.

Reviewed by Alvaro Moreira, MD as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn School of Medicine, Mount Sinai

On 2021-07-19 03:14:17, user Antônio Medeiros wrote:

Now published in EClinicalMedicine: https://doi.org/10.1016/j.e...

On 2020-05-26 15:37:05, user Sinai Immunol Review Project wrote:

Main Findings <br /> The authors describe a small cohort of 27 COVID-19 patients treated with enoxaparin or heparin in escalating doses (corresponding to clinical severity) at Sirio-Libanes Hospital in Sao Paolo, Brazil. Importantly, no control patients are included in this study. Additionally, all patients received concomitant azithromycin and a subset received methylprednisolone therapy. Patients had mean WHO score of 4.0 ± 1.2 (corresponding to moderate clinical severity) upon admittance. PaO2/FIO2 was significantly increased from 254 (±90) to 325 (±80) after 72 hours after the initiation of heparin therapy. 56% of patients were discharged within 7.3 (±4.0) days. 50% of mechanically ventilated patients were extubated within 10.3 (±1.5) days. The study reported no fatal events or bleeding complications due to anticoagulation. The authors suggest that early heparin therapy significantly improves hypoxemia and may be beneficial in the management of such patients.

Limitations <br /> This is a small, single arm, retrospective study without controls and with concomitant confounding treatments. Therefore, no definitive conclusions can be made here.

Significance <br /> This article adds anecdotal evidence regarding coagulability in COVID-19 patients and points to the potential for anticoagulation in the right clinical study. Given the multiple limitation, evidence herein can only corroborate previous reports demonstrating associations between elevated D-dimer and disease severity [1-3]. Additionally, this study may add to the evidence regarding mortality benefits of heparin therapy in severe COVID-19 [2, 3].

Credit <br /> Reviewed by Joan Shang as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn School of Medicine, Mount Sinai.

Reference<br /> 1. Han H, Yang L, Liu R, et al. Prominent changes in blood coagulation of patients with SARS- CoV-2 infection. Clin Chem Lab Med 2020 doi: 10.1515/cclm-2020-0188 [published Online First: 2020/03/17]

On 2019-11-30 17:00:40, user Guyguy wrote:

EVOLUTION OF THE EPIDEMIC IN THE PROVINCES OF NORTH KIVU AND ITURI AT NOVEMBER 27, 2019

Thursday, November 28, 2019<br /> • Since the beginning of the epidemic, the cumulative number of cases is 3,309, of which 3,191 are confirmed and 118 are probable. In total, there were 2,201 deaths (2,083 confirmed and 118 probable) and 1077 people healed.<br /> • 443 suspected cases under investigation;<br /> • 5 new confirmed cases, including:<br /> o 4 in Ituri in Mandima;<br /> o 1 in North Kivu in Mabalako;<br /> • 2 new deaths of confirmed cases, including:<br /> o 2 new community deaths in Ituri in Mandima;<br /> o No deaths among confirmed cases in CTEs;<br /> • No cured person has emerged from CTEs;<br /> • No health worker is among the new confirmed cases. The cumulative number of confirmed / probable cases among health workers is 163 (5% of all confirmed / probable cases), including 41 deaths.

NEWS

Three members of the Ebola Virus Epidemic response killed during an attack in Biakato, Ituri

• Following the attack on the sub-coordination of the Biakato response in Ituri on the night of Wednesday 27th to Thursday 28 November 2019, three members of the Ebola response teams in this sector lost their lives ;<br /> • It is a provider and a driver of the vaccination committee and another driver;<br /> • In addition to these three deaths, there are 7 wounded and 6 others with psychological disorders and extensive material damage.<br /> • A good number of these teams from Biakato were evacuated in three waves to Goma. As soon as they arrived, they were greeted by a coordination team led by Prof. Steve Ahuka, general coordinator, who also visited the wounded before going to inquire about the security conditions and accommodation of evacuees. He did not fail to comfort them.

VACCINATION

• The vaccination commission is in mourning. A service provider and a driver of his team were killed on the night of Wednesday 27 November 2019 following attacks at the Biakato base in Ituri;<br /> • 2nd day without vaccination activity with the 2nd J & J vaccine following the disorders initiated by young people related to the security situation in Beni;<br /> • 724 people were vaccinated, until Tuesday, November 26, 2019, with the 2nd Ad26.ZEBOV / MVA-BN-Filo vaccine (Johnson & Johnson) in the two health zones of Karisimbi in Goma;<br /> • Since the start of vaccination on August 8, 2018 with the rVSV-ZEBOV vaccine, 255,373 people have been vaccinated;<br /> • Approved October 22, 2019 by the Ethics Committee of the School of Public Health of the University of Kinshasa and October 23, 2019 by the National Ethics Committee, the second vaccine, called Ad26.ZEBOV / MVA-BN -Filo, is produced by Janssen Pharmaceuticals for Johnson & Johnson;<br /> • This new vaccine is in addition to the first, the rVSV-ZEBOV, vaccine used until then (since August 08, 2018) in this epidemic manufactured by the pharmaceutical group Merck, after approval of the Ethics Committee on May 20, 2018. has recently been pre-qualified for registration.

MONITORING AT ENTRY POINTS

• Sanitary control activities are disrupted in the towns of Beni and Butembo in North Kivu province following demonstrations by the population which decries killings of civilians;<br /> • Since the beginning of the epidemic, the total number of travelers checked (temperature measurement ) at the sanitary control points is 121,159,810 ;<br /> • To date, a total of 109 entry points (PoE) and sanitary control points (PoCs) have been set up in the provinces of North Kivu and Ituri to protect the country's major cities and prevent the spread of the epidemic in neighboring countries.

As a reminder, the recommendations of the MULTISECTORAL COMMITTEE OF THE RESPONSE TO EBOLA VIRUS DISEASE are as follows:

1. Follow basic hygiene practices, including regular hand washing with soap and water or ashes;
2. If an acquaintance from an epidemic area comes to visit you and is ill, do not touch her and call the North Kivu Civil Protection toll-free number;
3. If you are identified as a contact of an Ebola patient, agree to be vaccinated and followed for 21 days;
4. If a person dies because of Ebola, follow the instructions for safe and dignified burials. It is simply a funeral method that respects funerary customs and traditions while protecting the family and community from Ebola contamination.
5. For all health professionals, observe the hygiene measures in the health centers and declare any person with symptoms of # Ebola (fever, diarrhea, vomiting, fatigue, anorexia, bleeding).<br /> If all citizens respect these health measures recommended by the Secretariat, it is possible to quickly end this 10th epidemic.

On 2020-08-10 09:28:12, user OxImmuno Literature Initiative wrote:

https://www.immunology.ox.a...

On 2020-04-17 14:24:08, user Daniel Corcos wrote:

If nothing had been done, one would have expected at least 500,000 deaths from Covid-19 in the USA in less than one year.

On 2020-10-29 07:12:38, user reality tester wrote:

orange county prevalence 12% equates to 7.6 x higher than reported? 61,000 cases reported x 7.6 = 463,000 divide by 3.1 mil population equals 15% at least as of today... add 35% of those who have innate immunity as research published in Science and Nature indicates, and OC is at herd immunity threshold... no wonder hospitalizations are decreasing on 7 day moving averages, and daily deaths likewise dropping, despite more "cases" as tallied by positive swabs ...

On 2021-01-26 10:38:27, user ??u?????? ????????? wrote:

Hi,<br /> the UK, South African and the Brazilian virus mutations can alter the results/conclusions of the study?

On 2020-07-30 04:05:03, user Martijn Hoogeveen wrote:

In the v5 update: results of medical findings explaining the effects of allergens/allergies on influenza/COVID-19 are included. Methodological sensitivity analyses are added by including bootstrapped correlations and controlling for autumn. Outcomes are similar and conclusions are the same.

On 2020-03-26 16:04:12, user Sinai Immunol Review Project wrote:

Title: Meplazumab treats COVID-19 pneumonia: an open-labelled, concurrent controlled add-on clinical trial

Keywords: Meplazumab, CD147, humanized antibody, clinical trial <br /> Main findings: This work is based on previous work by the same group that demonstrated that SARS-CoV-2can also enter host cells via CD147 (also called Basigin, part of the immunoglobulin superfamily, is expressed by many cell types) consistent with their previous work with SARS-CoV-1. 1 A prospective clinical trial was conducted with 17 patients receiving Meplazumab, a humanized anti-CD147 antibody, in addition to all other treatments. 11 patients were included as a control group (non-randomized). <br /> They observed a faster overall improvement rate in the Meplazumab group (e.g. at day 14 47% vs 17% improvement rate) compared to the control patients. Also, virological clearance was more rapid with median of 3 days in the Meplazumab group vs 13 days in control group. In laboratory values, a faster normalization of lymphocyte counts in the Meplazumab group was observed, but no clear difference was observed for CRP levels.

Limitations: While the results from the study are encouraging, this study was non-randomized, open-label and on a small number of patients, all from the same hospital. It offers evidence to perform a larger scale study. Selection bias as well as differences between treatment groups (e.g. age 51yo vs 64yo) may have contributed to results. The authors mention that there was no toxic effect to Meplazumab injection but more patient and longer-term studies are necessary to assess this.

Significance: These results seem promising as for now there are limited treatments for Covid-19 patients, but a larger cohort of patient is needed. CD147 has already been described to facilitate HIV 2, measles virus 3, and malaria 4 entry into host cells. This group was the first to describe the CD147-spike route of SARS-Cov-2 entry in host cells 1(p147). Indeed, they had previously shown in 2005 that SARS-Cov could enter host cells via this transmembrane protein 5). Further biological understanding of how SARS-CoV-2 can enter host cells and how this integrates with ACE2R route of entry is needed. Also, the specific cellular targets of the anti-CD147 antibody need to be assessed, as this protein can be expressed by many cell types and has been shown to involved in leukocytes aggregation 6. Lastly, Meplazumab is not a commercially-available drug and requires significant health resources to generate and administer which might prevent rapid development and use.

1. Wang K, Chen W, Zhou Y-S, et al. SARS-CoV-2 Invades Host Cells via a Novel Route: CD147-Spike Protein. Microbiology; 2020. doi:10.1101/2020.03.14.988345
2. Pushkarsky T, Zybarth G, Dubrovsky L, et al. CD147 facilitates HIV-1 infection by interacting with virus-associated cyclophilin A. Proc Natl Acad Sci USA. 2001;98(11):6360-6365. doi:10.1073/pnas.111583198
3. Watanabe A, Yoneda M, Ikeda F, Terao-Muto Y, Sato H, Kai C. CD147/EMMPRIN acts as a functional entry receptor for measles virus on epithelial cells. J Virol. 2010;84(9):4183-4193. doi:10.1128/JVI.02168-09
4. Crosnier C, Bustamante LY, Bartholdson SJ, et al. BASIGIN is a receptor essential for erythrocyte invasion by Plasmodium falciparum. Nature. 2011;480(7378):534-537. doi:10.1038/nature10606
5. Chen Z, Mi L, Xu J, et al. Function of HAb18G/CD147 in Invasion of Host Cells by Severe Acute Respiratory Syndrome Coronavirus. J Infect Dis. 2005;191(5):755-760. doi:10.1086/427811
6. Yee C, Main NM, Terry A, et al. CD147 mediates intrahepatic leukocyte aggregation and determines the extent of liver injury. PLOS ONE. 2019;14(7):e0215557. doi:10.1371/journal.pone.0215557

Review by Emma Risson and Robert Samstein as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn school of medicine, Mount Sinai.

On 2021-11-05 19:55:40, user Mazen Baroudi wrote:

Now published by BMJ Open

On 2020-09-08 20:12:03, user Lewis Lee wrote:

Dear authors,

Many thanks for the interesting paper with numerous measures/analyses for controlling confounding. I'd like to ask the following:

How valid is it to use the set of the defined ICD-10 codes for identifying COVID-19 cases? I presumed the use of U07.1 (and possibly some U07.2) may only include those who were tested for the COVID-19. I guess majority of the general population were not tested. If that's the case, most of the COVID-19 negative cases may not be truly negative but indeed unobservable (missing data) at the moment of analysis. Besides, those who did the COVID-19 tests may have already different measured/unmeasured characteristics from the non-tested population as they were not randomly/probability sampled for tests. Could this be a source of selection bias/confounding and limit the validity and generalizability of the findings?

Many thanks and apologize if I missed some important details of the paper before asking.

On 2021-02-06 02:50:56, user Crystal Sonia wrote:

How accurate and reliable is this SIR model? With the mco arent the cases still increasing? How are the beta and gamma estimated? What's the sensitivity and specificity of this model?

On 2021-06-13 22:46:46, user Kenji Ikemura wrote:

Finalized peer-reviewed manuscript accepted by JMIR: <br /> https://www.jmir.org/2021/2...

On 2021-04-07 03:09:47, user Jesse Baker wrote:

I think Table 1 should list, for each age group and month, the actual number of cases and the number of people who were tested for Covid, as these quantities are needed to interpret the case fatality rates (CFR) given there. It is well known that the CFR generally decreases as more people are tested for the virus; the tests discover mild infections otherwise overlooked. If younger people were becoming less likely to seek testing while older people maintained their previous testing habits, this might explain at least part of the observed increase in the CFR and the bias toward younger ages.

I’m not an expert in such matters, and concern over the new strains P.1, B.1.351 and especially B.1.1.7 extends to the USA as they begin to circulate here. The April 6 New York Times noted an increase in hospitalization among Americans under age 50 during March, but it has yet to be reflected in case fatality rates for that group.

On 2025-07-09 03:42:51, user Alejandro Arbona wrote:

This preprint has been published https://doi.org/10.1016/j.jad.2024.12.030

On 2020-04-02 15:17:14, user Mc Uwamwezi wrote:

I have to say I am confused by the numbers, they say they enrolled 62 patients out of which 31 where given the HCQ treatment but then the results show outcomes for n=32 and n=32 respectively in the test and the control arms, so a total of 64??

On 2020-04-02 17:36:46, user antonio wrote:

It says two patients had adverse reactions to the treatment, maybe theyre missing for that reason

On 2020-04-09 06:55:47, user Cy Husain wrote:

Helpful study on "best available" (read: not very good) evidence for #hydroxychloroquine. In short, this study:<br /> - Is too small<br /> - Has no control group<br /> - Only looks at a very specific patient pool<br /> - Does not consider side-effects<br /> - It's NOT a double blind study, so allows for researcher bias!

On 2020-04-30 19:23:08, user Pei-Hui Wang wrote:

This work has been published on Journal of Medical Virology ( https://onlinelibrary.wiley... ). According to the findings in this paper, we propose that antibody-based COVID-19 “immunity passports” is unfeasible.

We agree with the opinions of Jayakrishna Ambati, Balamurali Ambati, and Benjamin Fowler that “ Passport holders and society would have a false sense of security while non–passport holders would have their civil liberties and work opportunities unwarrantedly abridged. A passport policy would also endanger lives by undercutting good hygiene and healthy behavior; those desperate to return to work or re-integrate into society would risk exposure to the virus in attempt to develop antibodies.” From Scientific American https://blogs.scientificame...

On 2025-08-26 09:13:00, user Constant VINATIER wrote:

Feedbacks about your preprint : https://doi.org/10.1101/2025.07.26.25332244

About registration: <br /> We could not find any information about the pre-registration of your study in the pre-print. Pre-registration involves documenting the hypotheses, methods, and/or analyses of a scientific study prior to its conduct (10.1073/pnas.1708274114; 10.1038/s41562-021-01269-4). If your study was pre-registered, we strongly encourage you to include the registration number in the pre-print, ideally in the abstract make this important information easy to retrieve, as this practice enhances transparency and reproducibility. If the study was not pre-registered, this should be acknowledged as a limitation. For future studies, we recommend pre-registering on an appropriate repository.<br /> About Protocol Sharing: <br /> We did not find the protocol for your study. If you have one, we encourage you to share it as supplementary material or deposit it in a publicly available repository such as the Open Science Framework ( https://osf.io ) or Zenodo ( https://zenodo.org/) "https://zenodo.org/)") . You can then include a statement in the Methods section indicating that your protocol is openly available (e.g., 'The protocol for this study is available at (link)/ in the supplementary'). Sharing your protocol will help readers better understand your study and enable them to reproduce it if they wish to test it.<br /> About the Statistical Analysis Plan Sharing: <br /> We did not find the Statistical Analysis Plan (SAP) for your study. If you have one, we encourage you to share it as supplementary material or deposit it in a repository such as the Open Science Framework ( https://osf.io ). You can then include a statement in the Methods section indicating that your protocol is openly available (e.g., 'The SAP for this study is available at (link)/ in the supplementary'). Sharing your SAP will help readers better understand your study and enable them to reproduce it if they wish to test it.<br /> About Deviations and/or changes<br /> We could not find any information about potential deviations or changes to the protocol in your pre-print. Since such deviations are common, if this applies to your study, we strongly encourage you to include a subsection titled Changes to the Initial Protocol in the Methods' section and discuss these changes as a potential limitation of your results. If any deviations occurred during your study, please specify them in this new subsection.<br /> About Data sharing / FAIR Data<br /> We found insufficient information about your data sharing approach. Data should be findable, i.e. data are assigned a globally unique and persistent identifier (for instance there is a DOI assigned to the dataset, or data are registered or indexed in a searchable resource). Data should also be accessible, i.e. data are retrievable by their identifier and can be accessed following an open, free, and universally implementable protocol. The protocol allows for an authentication and authorization procedure, where necessary. As your data contains sensitive data, we suggest to make it Findability, Accessibility, Interoperability, and Reuse ( https://www.go-fair.org/fair-principles/) "https://www.go-fair.org/fair-principles/)") by providing some details on this procedure.<br /> About Code sharing<br /> We could not find any information about your (statistical) code. Sharing code is important for enhancing transparency and reproducibility, especially since it does not contain sensitive information. We encourage you to openly share it on a code sharing platform (Github, Codepen, CodShare, etc.) and include the Digital Object Identifier (DOI) in the Methods section. If you want more information about Code sharing https://fair-software.nl/ .<br /> Comments :<br /> Dear authors, you state that 'All data produced in the present work are contained in the manuscript,' but we cannot find any link in your preprint or supplementary materials that refers to the protocol, code, raw data, and the registration number.

On 2020-04-07 22:42:22, user Christos Ouzounis wrote:

Spain 65,082 USA 267,324, estimated peaks.<br /> Today: 141,942 and 394,182 reported.<br /> Just a week later. Stats speak for themselves.

On 2020-12-01 21:55:11, user RRD wrote:

How does your model compare when it is based on a more infection disease (such as tuberculosis)?

On 2020-04-28 10:51:21, user Rosemary TATE wrote:

I have written a review of this preprint which can be found here<br /> https://outbreaksci.prerevi...

I hope you find it helpful and take some of my comments onboard before the next version.

On 2023-01-13 22:09:06, user WILLY CESAR RAMOS MUÑOZ wrote:

This paper has been published in Healthcare journal: https://www.mdpi.com/2227-9...

On 2021-10-15 07:29:10, user Rock Man wrote:

"So why on earth would anyone get a vaccine if they’ve already been infected?"

"You don’t get double immunity, or any ‘extra immunity’ at all."

That statement is not likely true. Just as the booster trials demonstrated when mixing firsts with different brand booster, there was a benefit. The same should be true between natural immunity and natural plus vaccines.

Re:

"The researchers found that those who got a Johnson & Johnson shot

followed by a Moderna booster saw their antibody levels rise 76-fold

within 15 days, whereas those who received another dose of Johnson &

Johnson saw only a fourfold rise in the same period. A Pfizer-BioNTech

booster shot raised antibody levels in Johnson & Johnson recipients

35-fold."<br /> https://www.nytimes.com/202...

On 2021-11-12 10:44:25, user Ken wrote:

The next step could be linking the TeKWP to the hospitalization rate in the ICU so to have a real time indicator on the stress that the structure can withstand in relation to the new cases

On 2020-05-11 12:28:29, user Sinai Immunol Review Project wrote:

The main finding of the article: <br /> This study analyzed the effects of the arterial hypertension and of the use of renin-angiotensin-aldosterone system (RAAS) inhibitors on mortality and recovery in patients with Covid-19. Through medical records, the authors performed a multicenter retrospective study of 3017 COVID-19 patients hospitalized within the Hackensack Meridian Health network in New Jersey. Among these patients, 52.5% presented a diagnosis of hypertension. The authors showed a significantly increase (2.7 times) of the mortality in patients with hypertension compared to Covid-19 patients without hypertension. However, when adjusted for age, the effect of hypertension in mortality decreased, as the incidence of hypertension was higher in older populations. In addition, when other clinical or demographic conditions were taken into account, no effect of hypertension on mortality was found. <br /> In relation to the RAAS inhibitors, angiotensin converting enzyme 1 (ACE1) inhibitors and angiotensin-receptor blockers (ARBs) were used in 22.8% and 18% of hypertensive patients. The use of ACE1 inhibitors and ARBs were found not to have detrimental effects and perhaps offer some protection to hypertensive patients in comparison with other anti-hypertensive agents. Hospital discharge rates were 9% higher for hypertensive patients prescribed RAAS inhibitors compared to other anti-hypertensive agents.

Critical analysis of the study: <br /> The manuscript needs a better scientific writing, especially more in-depth details on the description of the patient population, clinical parameters, treatments used, other co-morbidities. The implications for COVID-19 disease of the upregulated cascade of vasoactive peptides belonging to RAAS on hypertensive patients, the relationship between the use of RAAS inhibitors on cytokine storm, plasma angiotensin II and ACE2 activity, could be better discussed. There is no information on which ARBs or other anti-hypertensive agents were used, despite being an important information given the different pharmacological characteristics of each one.

The importance and implications for the current epidemics: <br /> While there is still uncertainty on the effect of RAAS inhibitors on Covid-19 severity in hypertensive patients, this manuscript demonstrates that ACE1 inhibitors and ARBs therapy are not detrimental, and can even be protective in hypertensive individuals. These results thus support the recommendations of the guidelines for maintaining therapy with these classes of drugs in hypertensive SARS-CoV-19 patients.

Reviewed by Bruna Gazzi de Lima Seolin.

On 2020-10-16 12:57:36, user Dieter Mergel wrote:

This article may help to explain a finding in:

https://www.medrxiv.org/con....<br /> Stipulating face mask wearing in Germany reduced the Covid-19 fatality rate although it did not affect the infection dynamics represented by the effective reproduction rate.

This is the most astonishing result of a data-scientific investigation: <br /> "Correlation between daily infections and fatality rate due to Covid-19 in Germany" and<br /> fits to the findings of 45% seroprevalence in Tokyo tempting to the breathtaking speculation that: <br /> "Wearing face-masks in densely populated areas is a sort of vaccination."

On 2021-08-06 23:22:56, user disqus_92pIDbtuHj wrote:

Hey, where's the full description of method and limitations? I get that this was published in medRxiv, a free distribution server for unpublished preprints that haven't been peer reviewed. It even states preprints "should not be relied on to guide clinical practice or health-related behavior and should not be reported in news media as established information".

This was a SMALL sample of 43 men... undergoing IVF and they served as their own self control. WHEN, was a sample after vaccination taken? WHEN was the baseline taken? HOW did they control for the effects of other variables... like the treatment recommendations these patients may have been following at the IVF clinic (especially since these were pulled Hospital IVF records)! They compared each man to his own baseline before and after vaccination, (14 men had male factor infertility, and 29 with normal spermogram results). Regardless all men were very likely receiving lifestyle, diet, or even medication recommendations! They also neglected to control season as a variable. Previous literature shows poorer sperm quality in Winter, and better quality in Spring. This design looked at two samples from each man somewhere between winter and spring. The same span of time for each man? No one knows!

On 2020-04-23 00:06:43, user Avi B Bhagan wrote:

The selection of the groups, does not seem random ,<br /> I don't see how this paper will get past peer review without revisions to remove about 20-25 patients from the analysis, in order to normalize the groups.

I don't know why the study group had nearly 20% smokers while the control group had closer to 12%. That is one source of expected higher mortality in the study group,

The other problem is the study group having the highest % of patients with complications from diabetes 30%, compared to 24% in the control group.

And 20% Cerebrovascular disease in the study group compared to 12% in the control group

And lastly why are patients with HIV, who would already be on other anti-viral drugs included in the study ? they should all be removed. This study has 4 patients with HIV in the control groups, and that is a blatantly dishonest move. the HIV patients who received "no medication" , would still be on HIV anti-virals , which is also a suspected treatment for COVID.

This analysis has to be re-run, to normalize for smoking, diabetes and heart disease, and removing the 6 HIV patients..

On 2020-04-24 12:11:44, user Mortal Wombat wrote:

Okay, you did this, but why? Is it really anything other than an overfit model?

Your original projections were off. You're never going to collect enough data for this to be falsifiable.

On 2020-04-15 11:57:26, user Renato Prandina wrote:

Duration and extent of immune protection will be critical to the novel betacoronavirus SARS-CoV-2 and will unfold in coming years. Some speculative scenarios...

On 2022-10-05 13:49:05, user Merja Rantala wrote:

Congrats for this preprint, it is an important summary what we know about protection of hybrid immunity and prior infection against cov19. However, I think that references and claims in the discussion should be checked. There was a sentence on page 13, first paragraph, claiming that covid survivors would have higher risk for dementia in addition to some other conditions. The reference cited was 36, which is not at all about risks for diseases after covid, but the other way around: risk factors for a severe covid outcome. So the ref need to be replaced. Moreover, we really don''t know at this stage whether risk for dementia is increased after covid or not, although has been under heavy speculation.

On 2020-06-02 15:13:39, user Sinai Immunol Review Project wrote:

Title <br /> Serum protein profiling reveals a landscape of inflammation and immune signaling in early-stage COVID-19 infection

Keywords<br /> • Serum Profiling<br /> • Cytokines<br /> • Protein array<br /> • CCL2<br /> • CXCL10

Main Findings<br /> In this preprint Hou et al., analyze serological immune mediators and other proteins from individuals with early COVID-19 symptoms using an antibody microarray that detects 532 target proteins. Patients were classified as COVID-19 (n=13) or influenza (n=15) based on positive RT PCR test for SARS-CoV-2 RNA (COVID-19) or FluA, FluB, RSV RNA (all classified as influenza group).<br /> 88 up-regulated and 37 down-regulated proteins were identified by comparing COVID-19 and influenza patient groups (p-value < 0.05). Some of those up-regulated ytyl34proteins were reported before, such as IFN-????, IL-6, CXCL8, CCL2, CXCL10 and some that were not previously associated with COVID-19, such as IL-20, CCL27 and IL-21. Complement proteins C1R and C7, as well as PLG were found to be reduced in COVID-19 patients.

After performing a correlation analysis of the differentially upregulated proteins and clinical data, the authors found a positive correlation between expression of several proteins in the CCL2 and CXCL10 signaling pathways and clinical parameters typically related to liver and renal function, myocardial injury, inflammation and infection, as well as neutrophils counts. Conversely, most of these same proteins show a negative correlation with lymphocyte counts.

Limitations<br /> The control “influenza group” had patients negative for influenza virus but positive for RSV, and thus the nomenclature should be revised. As noted by the authors, a larger cohort should be used to validate findings. There is no multivariate analysis, and identification of independent or confounding variables. Even though several proteins were differentially expressed between the patient groups, there was significant overlap between the groups, which may preclude the use of any single protein as a biomarker. Data on clinical variables should have been included in main figure. It is unclear why the authors annotated serum proteins in cellular components. Proteins in CCL2 and CXCL10 interaction network are largely overlapping, but the authors do not emphasize it. <br /> Authors didn’t show lymphocyte and neutrophil counts. Since it is known that severe COVID-19 patients can present lymphopenia and neutrophilia, it would be important to have this information in their cohort as they are correlating protein levels with neutrophils and lymphocytes.<br /> Authors claim that CCL2 can act as an autocrine factor that promotes viral replication in infected macrophages, and cite one paper with HIV, but authors should discuss that this chemokine recruits monocytes to the site of infection and then could contribute to the increased inflammatory response related to COVID-19.

Significance<br /> This study shows the potential use protein array to simultaneously identify many different proteins in serum of COVID-19 patients.<br /> The authors identify several differentially expressed proteins (potential biomarkers) and correlate them with clinical indices that give insights on possible therapy targets in COVID-19.

Credit<br /> Reviewed by Alessandra Soares-Schanoski as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn School of Medicine, Mount Sinai.

On 2022-09-23 18:40:11, user Andre Caldwell wrote:

This is an interesting paper, with an innovative study design which includes individuals with specific mutation and risk variants for Alzheimer's disease. <br /> I really wanted to like this paper, but after ready it in depth, just the study design is worth.<br /> 1) this study generated data in more than 1 million nuclei. After QC only 300K pass QC, meaning that more than 70% of the data was removed. when a study remove 70% of the data, it is not clear if what is left is reliable. This is very concerning indicating a large problem in nuclei extraction, batch effect or data generation.<br /> 2) the most common cell type on this study was oligodendrocytes which is totally unexpected. None of the other published studies using the technology has this finding. In fact, normally neurons is the most common cell type. This support that there is a large problem with this data.<br /> 3) the authors forgot to include a very basic comparison which is the major cell proportion vs. status. This is striking as the authors have a nice previous papers in which they do the same with deconvoluted bulk-RNA seq and single nuclei RNA-seq. No presenting this data is suspicious, as is it one the basic analyses and a good positive control.

Besides that, the paper is difficult to follow, tries to cover many things, but fails to go in any in detail or provide any interesting results, making the study very descriptive without providing clues about disease pathogenesis.

this paper have been as a preprint more than one year, suggesting that the authors are having problems to published these findings. May be the reviewers had several concerns.

On 2021-02-13 15:15:13, user Rick Phelps wrote:

It was noted that high degrees of in and ex leakage rates were typically observed. Were added filtration control measures taken to reduce and or control this variable. ? Others have published means by which the public can increase overall FFE using many techniques and materials.

On 2020-12-08 21:22:40, user Michal Piják wrote:

DOUBTS ABOUT THE EFFECTIVENESS OF MASS TESTING OF ASYMPTOMATIC POPULATION FOR CORONAVIRUS (SARS-CoV-2) IN SLOVAKIA

Indeed, it might seem that the number of positive PCR tests / per day, per million inhabitants two weeks after the nationwide testing of the whole country in Slovakia has started to slowly decrease. However, this declining trend may be skewed by significantly less testing. For example data from Monday 9.11.20 show that if as many tests were performed in Slovakia as on Thursday 29.10.20 (when the highest number of positives in the second wave was reached), we should have about 3x times higher number of positives on Monday 9.11.20. cases, i.e. about 3150, instead of 1050.

The cause of the lower number of tests is not known and one of the reasons could be the lack of RT PCR tests or staff in other days. After extensive testing with antigen tests, we had a big problem in Slovakia. This is that so far we have evaluated the situation according to the positivity of PCR tests. However, antigen testing made this situation unclear to us because people tested positive for antigens fell out of the statistics. It should also be borne in mind that lower numbers of positive cases could also be explained by the tightening of epidemiological measures and also because most of the persons with positive antigen tests were quarantined and did not undergo PCR testing.

There is evidence that strategies based on a large number of tests may not produce the expected results. A good example is a comparison of the strategies used by New Zealand and Iceland.1-2 In both of these island countries, the first cases were identified at the end of February 2020, but each country took a different path. New Zealand was one of the few countries that openly announced a COVID-19 elimination strategy right at the beginning of the epidemic. This included a gradually strengthened system for monitoring and isolating contacts with the timely and consistent use of lockdowns and border controls. It should also be recalled that some EU countries, such as Belgium, the Czech Republic, Switzerland, France, Slovenia and the Netherlands, have had a progressive decline in the number of positives, despite the fact that they did not have any comprehensive testing of the entire country.

Unlike New Zealand and many other countries, Iceland's strategy did not include any lockdown period, no official border closure for non-residents and negligible use of quarantine facilities. The cornerstone of Iceland's strategy was easy access to testing and mass screening, along with quarantine and contact tracking. According to data from October 21, New Zealand had 6 times fewer deaths, despite 4.5 times fewer tests than Iceland. Similarly, Slovakia, despite more than 8 times lower number of tests, had half less deaths per million inhabitants than Iceland. It should be recalled that, despite the large number of tests in Iceland, this was not a full-scale test and PCR tests were used. Taken together these findings are further evidence that nationwide antigen testing in a country with low prevalence is ineffective.

References<br /> 1. Jefferies S, French N, Gilkison C. COVID-19 in New Zealand and the impact of the national response: a descriptive epidemiological study. Lancet Public Health. 2020;5:e612-e623

1. Murdoch, D, Gottfreðsson M. COVID-19 and small island nations: what we can learn from New Zealand and Iceland., The conversation, published, September 23, 2020, https://theconversation.com...

On 2021-01-23 13:21:08, user Dušan wrote:

"All authors declare that they have no conflicts of interest"

Have a look at Jarcuška's organisation Euromedpro which is sponsored by GSK and Pfizer.

On 2020-03-26 13:52:15, user Sinai Immunol Review Project wrote:

SUMMARY: This study aimed to find prognostic biomarkers of COVID-19 pneumonia severity. Sixty-one (61) patients with COVID-19 treated in January at a hospital in Beijing, China were included. On average, patients were seen within 5 days from illness onset. Samples were collected on admission; and then patients were monitored for the development of severe illness with a median follow-up of 10 days].

Patients were grouped as “mild” (N=44) or “moderate/severe” (N=17) according to symptoms on admission and compared for different clinical/laboratory features. “Moderate/severe” patients were significantly older (median of 56 years old, compared to 41 years old). Whereas comorbidies rates were largely similar between the groups, except for hypertension, which was more frequent in the severe group (p= 0.056). ‘Severe’ patients had higher counts of neutrophils, and serum glucose levels; but lower lymphocyte counts, sodium and serum chlorine levels. The ratio of neutrophils to lymphocytes (NLR) was also higher for the ‘severe’ group. ‘Severe’ patients had a higher rate of bacterial infections (and antibiotic treatment) and received more intensive respiratory support and treatment.

26 clinical/laboratory variables were used to select NLR and age as the best predictors of the severe disease. Predictive cutoffs for a severe illness as NLR >= 3.13 or age >= 50 years.

Identification of early biomarkers is important for making clinical decisions, but large sample size and validation cohorts are necessary to confirm findings. It is worth noting that patients classified as “mild” showed pneumonia by imaging and fever, and in accordance with current classifications this would be consistent with “moderate” cases. Hence it would be more appropriate to refer to the groups as “moderate” vs “severe/critical”. Furthermore, there are several limitations that could impact the interpretation of the results: e.g. classification of patients was based on symptoms presented on admission and not based on disease progression, small sample size, especially the number of ‘severe’ cases (with no deaths among these patients). Given the small sample size, the proposed NLR and age cut offs might not hold for a slightly different set of patients. For example, in a study of >400 patients, ‘non-severe’ and ‘severe’ NLR were 3.2 and 5.5, respectively 1.

References:<br /> 1. Chuan Qin, MD, PhD, Luoqi Zhou, MD, Ziwei Hu, MD, Shuoqi Zhang, MD, PhD, Sheng Yang, MD, Yu Tao, MD, PhD, Cuihong Xie, MD, PhD, Ke Ma, MD, PhD, Ke Shang, MD, PhD, Wei Wang, MD, PhD, Dai-Shi Tian, MD, PhD, Dysregulation of immune response in patients with COVID-19 in Wuhan, China, Clinical Infectious Diseases, , ciaa248, https://doi.org/10.1093/cid...

This review was undertaken as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn school of medicine, Mount Sinai.

On 2021-02-24 20:56:12, user Dmitry Kobak wrote:

Thanks. Of course there is a PDF version -- you can click "Download PDF" above :-) Here is the direct link: https://www.medrxiv.org/con...

On 2021-06-11 03:08:36, user Kel Sigmund wrote:

1. Do you know if the relative lack of severe manifestations among the vaccinees with breakthrough covid 19 was associated with the occurrence of prior Covid 19 infection before undergoing vaccination?
2. Do you have data on the demographics of the vaccinee recipients, especially risk factors for severe disease and age because it would be interesting to know if the vaccine truly mitigated the severity of disease or the vaccinated population is younger and healthier than most being health care workers.

On 2022-01-10 10:57:41, user norsiiii wrote:

How can you study the rate at which unvaccinated and uninfected people had gotten infected? The rate, by definition, is 0 for all of them....

On 2023-04-20 05:53:06, user José F. Català-Senent wrote:

Hello everyone,

I am glad to inform you that the preprint has been published in the journal Neurobiology of Disease: https://doi.org/10.1016/j.n....

On 2021-11-07 19:02:49, user Sook Wah Yee wrote:

I see quite a few metabolites that I was interested previously found by Long T. et al. metabolomic GWAS (performed in >97% female) (https://doi.org/10.1038/ng.... "https://doi.org/10.1038/ng.3809)") not listed as significant in this male only mGWAS. This is interesting and wonder if there are gender specific mGWAS and whether comparison have been done?

On 2021-01-06 17:08:20, user Jeff Boris wrote:

I would be careful with your definition of POTS--it is not as rigorous as it should be. For adults, it really should be a relatively persistent increase of HR of at least 30 bpm in the first 10 minutes of standing after supine position, with symptoms of orthostatic intolerance, and with a history of symptoms for at least 3 to 6 months (depending on the reference). I do find the sex, race/ethnicity, and symptom distribution to be very similar to that of both our demographics article (Boris JR Cardiol Young 2018) and the Dysautonomia International-sponsored article (Shaw BH J Intern Med 2019).

On 2021-01-01 08:15:38, user Forrest Weghorst wrote:

Figure 7 would be more informative if the graphs showed symptom trajectories of Positive Tests vs. No Positive Tests (which is what all the statistical tests are comparing in the corresponding paragraph), not Positive Tests vs. Everyone (including Positive Tests).

On 2020-04-03 07:50:32, user BoghosLArtinian wrote:

In times of lethal pandemics any safe treatment that shows the slightest benefit should be tried before waiting for large scale scientific studies to be completed, to prove efficacy of treatments, and losing thousands of lives in the process.

On 2020-12-15 23:02:05, user E. de Moya wrote:

You should contact Mr. Wallukat and Celltrend, both researching autoantibodies in postviral Postural Tachycardia Syndrome (POTS) and ME/CFS. It would be interesting to see, if long-haulers also have amongst others, adrenergic and muscarinic aabs

On 2020-07-22 09:51:25, user Peiying Hong wrote:

what was the spiked SARS-CoV-2 in the recovery test? Is it the gene product or actual SARS-CoV-2? Given that the wastewater may contain SARS-CoV-2, how can recovery efficiency be determined without accounting for those SARS-CoV-2 that are already present in the sample?

On 2020-04-17 22:28:49, user Whatrdafax wrote:

What are the consequences of not making this drug available during a pandemic and large numbers of people die? The FDA has logically made an emergency approval for the use of the drug. Parallel paths are being pursued rather than letting people suffocate to death when potential cures supported by sound scientific reasoning and small clinical trials are already available. As far as fear of misuse, or people doing stupid things -those aren't valid reasons for blocking use of a life saving drug. Those are reasons why many drugs are prescription only.

Concern for the wheels of capitalism mass producing something that might not work? If there is a competing technology that shows greater promise you have a point. But there isn't. The next best, and possible future solutions, don't have the benefit of decades of use that hydroxychloroquine has. Those drugs have to first pass the barrier of safety testing -and even then are OK'd for dying patients right to try experimental drugs.

The one valid concern is to ramp up production to insure those already dependent on hydroycholorquine (lupus patients is one example) are not endangered. A big wad of cash to the company already making Panquil and companies making generic versions would be well spent so they can immediately boost production assuming the base ingredient supply is elastic.

On 2021-12-21 06:29:36, user Diego Hernandez wrote:

I am still saddened how little seroprevelance data is available at CDPH. I had my public records request rejected 3x for Megha Mehrotra's inaccurate Seroprevelance study that was cancelled in July 2021. Cancelled due to routine blood screening cancellation yet, it was not included as part of Tomas Aragon's public health order 1 Day after canceling CDPHs seroprevelance data releases.

I still do not have your modeling for the studies CDPH released. I doubt sending another 3 FOIAs will get me the results.

When I asked for updating Seroprevelance studies in California beyond August 2020 you linked me back to CDC interactive dashboard.

In August 21' you co-authored a paper with seroprevelance data back to August 2020.

The policies issued through this pandemic are not in line with the data available. If policy is being coerced on people it has to be within reason, knowing a VE drop off can be at 90 days or sooner, why force persons into destitution of employment for refusal of vaccinations.

The trend points toward seasonal vaccinations in late Sept and boosters in December... But that's not the policy and transparency CDPH offers the public.

I've moved on to other topics of interest but I have lost faith in transparency at CDPH in decision making.

On 2020-04-01 13:02:24, user Carlos Affonso wrote:

Congratulation for the amazing article ! <br /> Are the data image available ?

On 2025-01-03 16:28:46, user Karl Klein wrote:

This article has now been published in the journal Epilepsia: http://doi.org/10.1111/epi.18251

On 2020-05-26 21:10:36, user Renato Polimanti wrote:

Hi Rachel. Thanks for your feedback. It's a very good point. We are revising the paper to clarify this issue. It's correct that V30M is close to the cg13139646 site. However, this methylation site is assessed via a type II probe, which shouldn't be affected by the allele change. Additionally, we also see that other TTR mutations affect the methylation change at the cg13139646 site, independently from the V30M effect. Please let me know your thoughts about this.

On 2020-09-08 12:00:16, user Wendy Olsen wrote:

I noted that the assumptions going into this model are a consistent proportion of Overseas and Home students, and a similar size student body, as last year. In addition the cases arriving at UK campuses would be over half from UK Home Students. So even if the assumption of consistent proportion from Overseas turns out untrue, there is still the problem that having more UK Home students will bring more cases into the campuses. I also noted the summary, written by the authors:

Their core estimate is that "81% of the 163 UK Higher Educational Institutes (HEIs) have more than a 50% chance of having at least one COVID-19 case arriving on campus when considering all staff and students. Across all HEIs it is estimated that there will be a total of approximately 700 COVID-19 cases (95% CI: 640 - 750) arriving on campus of which 380 are associated from UK students, 230 from international and 90 from staff. This assumes all students will return to campus and that student numbers and where they come from are similar to previous years. According to the current UK government guidance approximately 237,370 students arriving on campus will be required to quarantine because they come from countries outwith designated travel corridors. Assuming quarantining is 100% efficient this will potentially reduce the overall number of cases by approximately 20% to 540 (95% CI: 500 - 590). Universities must plan for COVID-19 cases ... and ... reduce the spread of disease. It is likely that the first two weeks will be crucial to stop spread of introduced cases. Following that, the risk of introduction of new cases onto campus will be from interactions between students, staff and the local community as well as students travelling off campus for personal, educational or recreational reasons.

"COVID-19 has resulted in the on-campus closure of HEIs across the UK in March 2020 (1). Since that point universities have been working predominantly as virtual establishments with most staff working from home. Autumn sees the start of the new academic term with the potential return of more than 1.5 million UK and almost half a million international students (2).

"The COVID-19 pandemic continues ... approximately 1000 new cases reported each day in the UK, 25,000 across Europe and 250,000 worldwide ((3) accessed 28/03/20). There have been a number of outbreaks of COVID-19 reported in universities in the USA (The University of North Carolina, Notre Dame in Indiana, Colorado College, Oklahoma State and University of Alabama (4)) where the national infection rate is approximately 10 times higher than the UK (3). advice ...(5, 6). However, it is currently unknown to what extent COVID-19 will be brought to campus by staff and students whether from the UK or abroad."

On 2020-03-27 14:17:30, user Adam Roberts wrote:

Hello<br /> I would like to highlight the citizen science, antimicrobial discovery project, with the same name; https://www.lstmed.ac.uk/pu...<br /> All the best<br /> Adam

On 2020-06-09 18:29:42, user Chris Winchester wrote:

Would it be possible to study in your data set the quality of RCTs from different funders (e.g. commercial funders vs governmental funders, charities and NGOs)?

On 2022-01-20 04:04:11, user Andrew David wrote:

How can it be 100% effective against Delta for hospitalization or death with a confidence interval reported as 95% CI: 43.3-99.8 ?<br /> See results in the abstract.<br /> How can an estimate lie outside the confidence interval? <br /> I wish 100% could be true, but wishing doesn’t make it so. Or have math and statistics changed on account of Covid?<br /> That’s just plain sloppy.

On 2020-04-16 17:51:35, user James Bell wrote:

In the assumptions, was the ILI resulting from flu an average number or some lower number? This flu season peaked in November/December. A simple Google search reflects this through articles that were published about it at the time. If, in fact, an average ILI was used, doesn't that means the flu ILI are too high in this paper and that the overestimated value presumably belongs to COVID-19 instead? Also, since some in the media are arguing this paper "proves" we don't need the lockdown, is that really true (assuming all the assumptions in the paper are correct)? After all, we're talking about a virus for which none of us (except those who have recovered from it) have any immunity. If you have viruses with equal fatality rates, but we have herd immunity to one and not the other, doesn't common sense dictate there would be more fatalities with the latter (all else being equal)?

On 2024-01-11 13:59:49, user Mahalul Azam wrote:

This work now published in https://doi.org/10.15294/ke...

https://journal.unnes.ac.id...

On 2021-03-17 10:44:27, user Krisantha Weerasuriya wrote:

If there was the opportunity, a small simultaneous blood sample from the mother to measure the COVID19 antibodies would have provided further useful information.

Would it be possible with covering permission from the Ethical Committee to do a simultaneous blood sample for COVID 19 antibodies from mother and baby at 3 months (or the most appropriate time)?

On 2020-04-15 14:34:21, user Bio wrote:

I have several issues with this study:

1. I find not including time as a factor in the model bewildering. After all, time is the single most important factor for the number of cases for most of the countries in the model. The model is only log(cases) ~ population + temperature. But for example, in half a month's time, population and temperature won't change much, while the number of cases could increase several fold for some countries. Time is a critical factor to model and is more important than temperature and population. Not including time, the model in the paper cannot be stable. Basically as time changes, your conclusions likely will change.

2. Many other important factors were not considered. For example, at what point of COVID-19 growth is each country at? If one compares March 14 to March 27, China's numbers are not much different while USA and many other countries have quite different numbers on those 2 days. The model cannot be stable due to this as well (time + point during growth). Also what about containment policy causing slower growth? Effects from such important confounding factors were not considered in the model.

3. There are many other smaller issues such as USA cases were mostly in Northeast, with latitude clearly higher than the one used to represent USA. In China, the cases happened in many provinces with vastly different latitude/temperature but all cases counted at one latitude/temperature. Moreover, the vast majority of the cases happened in China during Jan/Feb while you used late March temperature to represent them. Inaccuracies like these seriously impact modeling latitude/temperature as a continuous variable. Excluding countries with small population but high case rate as outliers is also questionable, given that you modeled population size already.

Fig. 7 could benefit from being plotted also for 2/29, 3/14, 3/21. Interpretation of Fig. 7 could instead be that it showed 2 groups of countries/latitudes that reflects the temporal sequence of events rather than temperature: COVID-19 started in China, spread to South Korea and Italy, then Europe and America as they trade/travel often and happen to all be cold countries; then in March COVID-19 picked up in southern hemisphere and tropical area and still going. It's likely time and policies that helped Australia case rate be relatively low instead of temperature, because the spread of COVID-19 is still early there and they learned from other countries to control the spread from early on.

Therefore I do not believe the paper provided convincing evidence for temperature-dependency of COVID-19.

On 2020-04-26 13:05:40, user Bin_Pei wrote:

Thanks for kind reminder of the reviewers, there is an unintentional editing error that we accidentally mixed the name of two cities in affliation in the original manuscript. We have submitted a revision already, there might be few days delay and we will be more careful in the future work.

On 2020-04-27 04:52:01, user Krishna Undela wrote:

It is the first information on knowledge and beliefs of general public of India on COVID-19. In this article we can understand the false beliefs / myths circulating among the general public of India about transmission of novel coronavirus and prevention and treatment of COVID-19.

On 2022-01-13 13:16:50, user Zacharias Fögen wrote:

Table S9 and S8, community median income, number of cases in <50,000 is higher in S9 than in S8, which is impossible. Same but reversed for 50,000-99,999, maybe exchanged numbers?<br /> Why in Table 3 did you use log increase for median income? that makes no sense to me, as you are using steps of 50,000 each.

However, more importantly, <br /> Table S3: HR Age per 1y increase =1.05 , that's not plausible as COVID-19 risk increases exponentially (doubles every 6-7 years). Using a linear regression on a nonlinear variable is not a fitting model. you could have used log age.

On 2021-04-20 16:21:52, user Laurie B wrote:

Thank you for conducting this important research work and making your results available online. This information must be widely communicated. My dad received his final Retuxin infusion January 2021. Shortly after he received Covid vaccination 1 and then February 4th the second. While still following most covid precautions he had certainly let his guard down as a "fully vaccinated" person. Turns out, he was not. He is in the ICU with covid. Please pursue a press release. Please let me know how I can help disseminate your findings. Thank you for your work!

This is how our family found out: https://www.nytimes.com/202...

And from an ICU Doc who shared: "Rituximab specifically target cancerous B cells and helps our immune system destroy them. But B cells are the very cells that make our antibodies so his response to the vaccine is going to be muted with or without the Rituximab."

On 2022-01-10 23:36:13, user Fred Ledley wrote:

A peer reviewed version of this work was published in Vaccine in 2021. https://www.sciencedirect.c...

On 2021-07-05 12:11:26, user Meerwind7 wrote:

Data from the US in 2020 showed a clear increase of cases in the southern states during summer, i.e. when and where air conditioning was the most widespread. After the summer heat, cases started to increase from North to South. Therefore, it seems quite obvious to me that air exchange is the main culprit of temperature- or weather-related changes.

Too complicated: "A further complication is that temperature, humidity, and UV radiation plausibly affect transmission and incidence through a range of biological and epidemiological mechanisms"

My theory could be further assessed by looking at regions or in sociological groups where installations of air conditioning are less widespread, so that people spend more time with open windows or outdoors in summer. A heatwave in temperate Europe (where air conditioning is rare in residential buildings) or in poor quarters of the US thus should not lead to increased infections, while a heat wave in US suburbs with widespread availability of air conditioning would have that effect (as long as people do not met outdoors anyway, in consideration of Covid-19). In southern Europe, air conditioning may be more widespread in urban centers, whih form heat islands, than in rural areas, so that would also drive differences,

On 2021-10-20 01:13:14, user rferrisx wrote:

The PHD hesitant numbers were adjusted for v2?:<br /> https://www.medrxiv.org/con...<br /> Page 24 table PHD:<br /> 23.9 (22.7, 25.1)v1<br /> 14.6 (13.5, 15.6)v2

On 2021-01-22 14:40:19, user Tim Meyer wrote:

It is understandable that the issue of the Covid-19 incidence in football (soccer) players is of general (and scientific) interest. Also, it makes sense to compare this incidence to the general population of that age. However, such comparisons have to be made in a scientifically sound manner. One of such principles - also on pre-print servers or possibly even more so on such platforms which are not peer-reviewed in advance - is the meticulous description of the methods being used. Unfortunately, crucial information about this is lacking for the article from Andersen et al. entitled „Incidence and relative risk of infection with SARS-CoV-2 virus (Covid-19) in European soccer players“.

It is not described how the infection numbers for the 5 leagues have been obtained (i. e. uncertainty about the numerator for the incidence calculation). Also, we do not get sufficient information about how the (estimated) incidence in the general population has been assessed. In this regard, it is noteworthy that a frequently tested population like the one of the players potentially has a number of undetected infections close to zero. This is completely different in the general population where some studies point to numbers of undetected infections in the range of 75-90% with higher values in the young age groups where asymptomatic Covid-19 courses are more frequent. Due to the very short methods description it is not clear which calculations have been carried out for this study. Therefore, we have uncertainties about the numerators of both incidence calculations which makes results hard to interpret.

When we assume (in favour of the authors´ numbers) that the number of undetected infections has been taken into account appropriately by referring to an „infection fatality rate“ from a small area in Germany (a highly questionable method from our perspective) the message would be that hygiene protocols in Germany and England work well. However, studies based on procedures like the ones in this text appear methodologically unsound and should not be published – not even on pre-print servers. Even on such pre-print platforms more thorough descriptions as well as careful interpretations (including the limitations of one´s work) are needed because otherwise misinterpretations may enter the public domain.

Tim Meyer (Conflict of Interest: Chair of the German Task Force "Sports Medicine/Special Match Operations" which has been developing the hygiene protocol for the German football leagues; chair of the medical committees of the DFB and UEFA); Barbara Gärtner (Conflict of Interest: Member of the German Task Force "Sports Medicine/Special Match Operations" which has been developing the hygiene protocol for the German football leagues

On 2020-03-24 14:01:51, user Sinai Immunol Review Project wrote:

Main findings<br /> The authors collected data on 25 COVID-19 patients (n=11 men, n=14 women) using standard laboratory tests and flow cytometry. All patients were treated with antibiotics. Twenty-four of the 25 patients were also treated with anti-viral Umefinovir and 14 of the patients were treated with corticosteroids. 14 patients became negative for the virus after 8-14 days of treatment. The same treatment course was extended to 15-23 days for patients who were still positive for the virus at day 14. <br /> The authors found a negative association between age and resolution of infection. Patients with hypertension, diabetes, malignancy or chronic liver disease were all unable to clear the virus at day 14, though not statistically significant.<br /> Elevated procalcitonin and a trend for increased IL-6 were also found in peripheral blood prior to the treatment.<br /> A trend for lower NK cell, T cell and B cell counts in patients was also reported. B cell, CD4 and CD8 T cell counts were only increased upon treatment in patients who cleared the virus. NK cell frequencies remained unchanged after treatment in all the patients.

Limitations of the study<br /> 73% of the patients who remained positive for SARS-CoV2 after the 1st treatment, and 43% of all patients who cleared the virus were treated with corticosteroids. Corticosteroids have strong effects on the immune compartment in blood{1}. The authors should have accounted for corticosteroid treatment when considering changes in T, NK and B cell frequencies.<br /> Assessing if IL-6 concentrations were back to baseline levels following treatment would have provided insights into the COVID-19 cytokine storm biology. Patients with higher baseline levels of IL-6 have been reported to have lower CD8 and CD4 T cell frequencies{2}. Correlating IL-6 with cell counts before and after treatment would thus have also been of interest.<br /> The report of the laboratory measures in table 2 is incomplete and should include the frequencies of patients with increased/decreased levels for each parameter.<br /> Correction is needed for the 1st paragraph of the discussion as data does not support NK cell restoration upon treatment in patients who cleared the virus. NK cells remain unchanged after the 1st treatment course and only seem to increase in 2 out of 6 donors after the 2nd treatment course in those patients.

Relevance<br /> Previous reports suggest an association between disease severity and elevated IL-6 or pro-calcitonin concentrations in COVID-19 patients3,4. IL-6 receptor blockade is also being administered to patients enrolled in clinical trials (NCT04317092). This report thus contributes to highlight elevated concentrations of these analytes in COVID-19 patients. Mechanisms underlying the association between viral clearance and restoration of the T cell and B cell frequencies suggests viral-driven immune dysregulation, which needs to be investigated in further studies.

References

1. The CHI Consortium et al. Effects of Systemically Administered Hydrocortisone on the Human Immunome. Sci Rep 6, 23002 (2016).
2. Zhao, Z. et al. Clinical and Laboratory Profiles of 75 Hospitalized Patients with Novel Coronavirus Disease 2019 in Hefei, China. http://medrxiv.org/lookup/d... (2020) doi:10.1101/2020.03.01.20029785.
3. Chen, X. et al. Detectable serum SARS-CoV-2 viral load (RNAaemia) is closely associated with drastically elevated interleukin 6 (IL-6) level in critically ill COVID-19 patients.<br /> http://medrxiv.org/lookup/d... (2020) doi:10.1101/2020.02.29.20029520.
4. Lippi, G. & Plebani, M. Procalcitonin in patients with severe coronavirus disease 2019 (COVID-19): A meta-analysis. Clinica Chimica Acta 505, 190–191 (2020).

Review by Bérengère Salomé as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn school of medicine, Mount Sinai.

On 2020-09-04 21:26:30, user Samir Arbache wrote:

Dear authors. Interesting essay, I am very interested in this subject. I made these injections at a specific point in the dermis of my forearm for 20 days (once a day), the skin came to ulcerate. After healing, I made a manual touch on the area but I didn't feel that the skin was hardened, so I avoided the biopsy. My question is: after the treatment of the rats, did you feel touching if the skin was hardened as morphea?

On 2020-05-21 01:21:24, user Morat Gurgeh wrote:

This whole affair has been entirely unedifying. I do not know the truth of the allegations published in Buzzfeed, but then neither does anyone else commenting here, on Twitter and elsewhere. There are a lot of people, including senior academics, who should be ashamed of their behaviour.

Turning to the central controversy, it is entirely possible and indeed likely for different populations to have different IFRs. The fact that the IFR in NYC appears to be significantly higher than reported here does not “debunk” this work and indeed is not even inconsistent with these results.

NYC was hit early by the virus, when protocols for managing infected patients were still developing and mistakes were made. In addition, those most susceptible to COVID-19 (e.g. the old) were much less likely to be voluntarily shielding. Catastrophic errors have been made in many countries in care homes. So the likelihood of those over 80 being infected was likely much higher than in this study. Given the incredibly steep fatality gradient with age, this alone could explain the IFR differences.

I think the main take home message of this paper is this: the lives of healthy, working age people should return largely to normal while those groups identified at elevated risk should continue to shield. Amongst the young, we should treat infection by SARS-CoV-2 as more akin to measles than Ebola.

We need most of the healthy, young population to develop what immunity they can to this virus so that we can properly protect those most susceptible.

On 2020-05-01 18:41:24, user LOLUVA wrote:

Looks like its lowered to 23x(unweighted) to 54x(weighted)

On 2020-04-08 15:07:01, user Georgeta Vaidean wrote:

Interesting paper. Good to see adjustment for 16 covs. and sens analysis. Any chance to add data on COPD, Lung cancer, CHD? both prevalence and mortality rates? particularly longitudinal figures (against historical background). Data are likely available, even at county level.

On 2022-02-15 20:38:21, user Outletshopping Bym wrote:

hello please how did you collected the data from social media?

On 2020-09-13 07:31:07, user OxImmuno Literature Initiative wrote:

https://www.immunology.ox.a...

On 2021-04-25 15:33:39, user Tam Hunt wrote:

This study is conflating deaths with covid with deaths caused by lockdown measures bc it employs the UK standard definition of a covid deaths as follows:

In the UK, all-cause death by 28-days post confirmation of SARS-CoV-2 infection is the standard definition of SARS-CoV-2 mortality,8 so we used death from any cause as the primary outcome. In sensitivity analysis restricted to people diagnosed with SARS-CoV-2 a minimum of 28-days prior to the censoring date, and logistic regression with deaths censored beyond 28-days the results were consistent.

On 2021-11-28 19:40:54, user Robert van Loo wrote:

44 relevant new variants up till now and on average some 2 per 10 million cases. Did we only see 220 million cases globally? I would think more with over 5 million deaths and an IFR of 0.6 %. I have papers and also WHO stating the reported 260 million cases is factors lower than the real number of infections. With over 5 million reported deaths and an IFR of 0.6 % the real number of infections would be over 800 million cases. The number of relevant new variants per 10 million cases would then be about 4 times lower. Of course if reported cases always underreport to the same extent the extrapolation of reported cases to new variants would not change. Still important to make the distinction as the underreporting factor is hugely variable.

On 2020-10-28 17:53:21, user Sam Wheeler wrote:

It it so that non-vaccinated hospital personnel are forced to wear a mask almost all the time to prevent flu, so the protection of flu vaccine is even greater than this study tells?

On 2021-02-24 22:16:27, user Long Nguyen wrote:

Hello. This paper has been published at https://pubmed.ncbi.nlm.nih... <br /> Thank you!

On 2021-05-27 04:54:05, user rusbowden wrote:

Not satisfied with my response from 11 hours ago being nearly as curt as what I responded to, I've come up with a list of links for anyone who wants to be up-to-date on how we have come to know about the efficiacy of wearing face masks. My hunch is that most readers here do not need it, but for anyone unfamiliar, it just seemed too vital to let lie.

Each article below includes the knowledge that masks are used to lessen aerosol transmission. What gets covered is what we know about how effective different types of masks are, how they should be worn. We also know how double masks help, what the research shows us there, and which mask should go on top, things like that. A recent article scientifically addresses Texas' executive orders, the harm done. But the final one, is the link to the the report that I was quoting from a day ago, that seriously undercuts this study.

Many readers will already recognize some if not most of the links. All of them need to be explained by anyone who wants to now say that all the science we've had and have been developing for over a year has been hogwash, that tjhousands of researchers have not know what they are talking about, that we now know none of it had veracity. We don't just go back to flat earth, because someone writes a research paper. Here they are:

To mask or not to mask: Modeling the potential for face mask use by the general public to curtail the COVID-19 pandemic<br /> https://www.ncbi.nlm.nih.go...

Masks Do More Than Protect Others During COVID-19: Reducing the Inoculum of SARS-CoV-2 to Protect the Wearer<br /> https://link.springer.com/a...

Will an imperfect vaccine curtail the COVID-19 pandemic in the U.S.?<br /> https://www.ncbi.nlm.nih.go...

Could masks curtail the post-lockdown resurgence of COVID-19 in the US?<br /> https://www.ncbi.nlm.nih.go...

Effectiveness of Face Masks in Preventing Airborne Transmission of SARS-CoV-2<br /> https://www.ncbi.nlm.nih.go...

Maximizing Fit for Cloth and Medical Procedure Masks to Improve Performance and Reduce SARS-CoV-2 Transmission and Exposure, 2021<br /> https://www.cdc.gov/mmwr/vo...

Impact of Public Health Education Program on the Novel Coronavirus Outbreak in the United States<br /> https://www.frontiersin.org...

Assessment of the COVID-19 Vaccine Program: Impact of the No Mask Mandate Executive Order in the State of Texas<br /> https://www.medrxiv.org/con...

What factors have determined how well countries have done in responding to the pandemic?<br /> https://richardswsmith.word...