On 2020-06-23 21:57:17, user Dr. D. Miyazawa MD wrote:

Please give me your opinion or point out any problems with this article.

On 2020-04-16 23:17:24, user Samantha Grist wrote:

We appreciate the authors’ urgency in addressing SARS-CoV-2 decontamination for reuse of N95 filtering facepiece respirators (FFRs). In the spirit of that urgency and health impacts, we note two concerns with the current preprint that could (unintentionally) cause confusion: (1) likely mismatch between the wavelength range to which the reported UVA/B light meter is sensitive and the viral-killing UV-C wavelengths emitted by the LED High Power UV Germicidal Lamp, as highlighted by other commenters, and (2) omission of a direct comparison between the UV-C doses applied in this study and the minimally acceptable UV-C dose understood to be needed for efficacy (e.g., CDC Guidance).

We have contacted the authors Fischer and Munster via separate email suggesting that they:

1. Please check a potential mismatch between the UVGI light needed for viral inactivation and the UVA/B light meter used: The LED High Power UV Germicidal Lamp described in the Methods emits in the 260-285 nm range, as is appropriate to inactivate virus by damaging DNA and RNA. However, the UVA/B light meter (General Tools) mentioned in the Methods section is not suited to detect the virus-killing light from the LED High Power UV Germicidal Lamp. Further supporting the possibility of a sensor-source mismatch is the reported irradiance of 5 µW/cm^2, which is ~1000x lower than typically reported for effective N95 FFR decontamination [Lore et al., 2012 (1.6-2.2 mW/cm^2); Heimbuch & Harnish, 2019 (4.2-18 mW/cm^2), Mills et al., 2018 (17 mW/cm^2)].

Being designed for germicidal function, the LED High Power UV Germicidal Lamp would have significant output in the UV-C range and would not be expected to have significant output in the UVA/B range (280-400 nm). Put another way, the UVA/B light meter used would not be able to accurately assess the germicidal function of the LED High Power UV Germicidal Lamp, which stems from the UV-C light. It is the UV-C-specific dose that is relevant to viral inactivation, with UV-B (280-320 nm) dose providing significantly lower germicidal efficacy, and UV-A (320-400 nm) considered very minimally germicidal [Kowalski et al., 2009; Lytle and Sagripanti 2005; EPA].

1. Please clarify the total UV-C dose delivered in Figure 1, as the peer-reviewed literature points to UV-C dose of > 1.0 J/cm2 as the critical factor in N95 FFR viral inactivation treatment. Although UV-C dose governs viral inactivation, the preprint does not clearly state the germicidal UV-C dose delivered to the N95 coupons for the Figure 1 treatment times. While germicidal UV dose is the product of the UV-C irradiance and exposure time, comparison to the minimally acceptable UV-C dose of 1.0 J/cm^2 is needed. UV-C irradiance varies significantly both between and within systems, so treatment time is not an accurate characterization metric for understanding UV-C germicidal efficacy (especially when translating to a different dosing system); dose needs to be quantified directly with a NIST-traceable, calibrated radiometer matched to the germicidal wavelength range of the source. At the reported 5 µW/cm^2 irradiance, the total dose delivered during a 60 min treatment period is only 18 mJ/cm^2, greater than an order of magnitude lower than the effective 1.0 J/cm^2 UV-C dose reported in the literature for similar viruses [Lore et al., 2012; Heimbuch & Harnish, 2019, Mills et al., 2018] and current CDC guidelines for UVGI decontamination of N95s [CDC]. A UV-C dose of 1.0 J/cm^2 across all N95 FFR surfaces is understood from the literature as the minimum acceptable for N95 decontamination.

Without these clarifications we are concerned that this important study may be misconstrued by readers as indicating that either (i) very low UV-C doses are sufficient for N95 decontamination (the peer-reviewed evidence suggests that they are not), (ii) a certain UV exposure time is sufficient for N95 decontamination (dose, not time, is the critical factor) or (iii) that UV-A or UV-B are effective decontamination wavelength ranges (they are not). In the spirit of the authors’ study, our #1 concern is for the health of our heroic healthcare professionals. For additional detail from the peer-reviewed literature, please see the 2020 scientific consensus summaries on N95 FFR decontamination at: n95decon.org.

On 2021-08-17 14:22:29, user Jon Hillman wrote:

'Taken together our results indicate that state implemented NPIs can lead to less COVID-19 cases and mortality.' How much less? CDC concluded it was no more than 1.8% reduction in cases: https://www.cdc.gov/mmwr/volumes/70/wr/mm7010e3.htm Quantifying the reduction matters to anyone concerned with objectively measuring NPI cost vs outcomes.

On 2021-10-25 17:08:33, user Arron190 wrote:

It would be interesting to see how the data changes if those with naturally acquired immunity (ie been infected) are removed.<br /> Around 13% of US citizens have been infected so far.<br /> Many of the uninfected may be interested to know what level of protection the vaccine provides.

On 2021-01-24 20:42:28, user Thomas Arend wrote:

Just some short remarks to table 5:

(35-5)/35 is 85.71% and not 82.86%

If you round 32/23 = 91.4285.. you get 91.43 not 91.42

Typo? 34/35 = 97.1428 ~ 97.14 ... not 97.12

And I agree with Michel Schrader comments to the presicion of 4 digits.

The hypothesis H0: specifity = 94% / Ha: specifity <> 94% you can only be rejected for AgPOCT V. p=0,0168.

H0: Specifiy = 92% cant be rejected for any AgPOCT.

You should calculate a CI for the specifity.

On 2021-11-20 00:18:36, user Scott_CA wrote:

Perhaps an explanation(or logical speculation) would be that Pfizer, Moderna, etc engineered and tested the vaccine based on the viral DNA of particular variants--a chemical 'best' fit that would probably be proprietary info. Because they have that capability, the vaccine may change in the future as the variants change.

On 2021-10-14 04:44:33, user gzuckier wrote:

The point of the study being infection covid, dropping those in one arm of the study who already died from covid when they entered the study is definitely to the point.

On 2021-10-28 00:09:07, user n0b0dy0fn0te wrote:

I'm with you on this. The lack of control for NPIs is a huge red flag, and means we have to treat the conclusion with a high degree of circumspection.

Imagine a study done in a school. Every day, every child in the school is given a meal containing precisely 1,000 calories. On careful analysis after a period of time, the study measures weight gain in all of the students, albeit by differing amounts from student to student. The study concludes that 1,000 calories per day is too much.

Then you notice that study, in listing its limitations, declares up front that they didn't control for the notion that the children might also be getting food from somewhere other than school. You'd have to treat the conclusion of the study with a good deal of circumspection, and you'd be remiss if you allowed the conclusion of this study to inform your dietary recommendations for schoolchildren.

That's what that lack of control does here. I mean, can anybody think of a reason that somebody who's been hammered by a moderately symptomatic case of COVID might be more inclined to maintain mask-wearing, physical distancing and other mitigations?

This paper will almost certainly not pass peer-review, and certainly not without significantly revision, revision which is going to be difficult, given the nature of the study. That lack of control makes this one of the shoddiest bits of experimental design I've encountered in a very long time as a science writer.

On 2021-08-28 02:02:31, user Marxtinks wrote:

It is not surprising that natural infection elicits stronger immune responses than the current vaccines. Covid 19 encodes 24 individual proteins. In contrast, only a single protein, the Spike antigen used by both Moderna and Pfizer in their vaccines. Furthermore, it is likely that the large scale S antigen mRNA immunization will lead to development of mutant strains not neutralized by sera or T cells of people vaccinated by the S antigen. It would be wise to develop novel vaccine strategies

On 2021-09-09 04:36:47, user Salvatore Chirumbolo wrote:

Dear Colleagues, my congratulations for this valuable and excellent paper. With a Colleague of mine, Sergio Pandolfi (Rome) we too addressed the topic of natural immunized subjects against SARS-CoV2 (see Pandolfi S, Chirumbolo S. On reaching herd immunity during COVID-19 <br /> pandemic and further issues. J Med Virol. 2021 Sep 7. doi: <br /> 10.1002/jmv.27322. Epub ahead of print.) but we highlighted also the controversial issue of the immunization route, i.e. mucosal versus intramuscular, I mean sIgA-B cell mediated respect to a DC-mediated immunity towards the IgGs production, with obviously different B-cell memory. Do you think that this is one of the major differences between immunized vs vaccinated people? And if serum anti-RBD IgGs are the only clue for evaluating immunized people, why a "certain" discriminating attitude exists towards natural immunized subjects respect to vaccinated ones?

Many thanks in advance<br /> Regards<br /> SC

On 2021-10-08 13:13:27, user Richard S wrote:

Did the authors address multicollinearity of the highly correlated independent variables in their regression models?

On 2021-08-27 10:52:36, user Sock Dollager wrote:

Please follow up on this comparing infectiousness / viral load of someone with two shots who gets breakthrough infected, vs infectiousness / viral load of prev infected/natural immunity patient who gets breakthrough infection.

Thank you.

On 2022-01-04 21:14:17, user Ed Hernandez wrote:

This is an observational study not double blind randomized and controlled. Not even worth a cent.

On 2021-09-09 09:59:21, user Patricia wrote:

This is one of a many studies that confirm what we already know, and that the CDC has confirmed, with >50% infected not knowing they are infected and being asymptomatic. Of those with symptoms, 80% are mild with cold-like symptoms and 80% of deaths are elderly. The US has a 1.6% death rate with SARS2, far below Peru's 9.2% or Mexico's 7.8% or Sudan/Syria 's 7.4% - out of 200 countries, the USA ranks #85/86 in the world. That is most likely due to the CDC refusing to support any safe COVID treatments successfully used around the world, the Media and Politicians condemning and smearing safe treatments (even banning use in multiple states), and the DO NOTHING APPROACH of : if you are really sick and need medical attention, quarantine and do nothing until you are on death's doorstep and need an ambulance & ventilator. Physicians that defied the nonsense & political hatred, by saving lives and treating COVID with very safe FDA approved drugs - with the common practice of off label use to treat the symptoms - show extremely low deaths rates. Excluding the CDC's push to use the very expensive Gilead's Remdesivir intravenously in Emergency settings that has a 2/3 success rate and ZERO STUDIES or Vanderbilt's monoclonal antibodies - There are over 1,000 studies with over 35 easily accessible drugs, that ALL PROVE INCREASED IMPROVEMENT. So why did the CDC and Doctors discourage any treatment and push the DO NOTHING UNTIL YOU ARE ALMOST DEAD PROTOCOL? In 21 months, since the first death in January 2020, 12% of the US Citizens have tested positive. >80% have mild to moderate symptoms. We have no idea how many had SARS2 because we have no idea how many more were asymptomatic. However, the CDC estimates 114.7M Americans have had SARS2 and have natural immunity. According to far left Media sites, the worst states to manage COVID are those with >200 cases per million, NY 349, NJ 284, SC 273, NV 237, DE 221, DC 209, MA 207 per million population. The most heavily populated states were the first states to be afflicted with COVID - 39M CA & 30M TX hovered around 97 per million, despite having highly criticized opposite approaches of CA Strict Lockdowns versus Texas Open with common sense guidelines. Since that revelation, COVID tracking was suspended by many or dates cherry picked when it became popular to smear successful states to deflect from the fact that the vaccine do not work and hence - are not a vaccine. They never said it would stop the disease, just somehow promised people wouldn't have as severe symptoms. Like treating flu with medicine to ease the symptoms for recovery. The US dismisses the chaos around the world, MSM refuses to inform us on major protests around the world that have been occurring for months. Why isn't the Oxford Director of Vaccines statement on every paper and news segment? He confirmed the vaccine isn't stopping SARS2 and herd immunity with it is "unachievable" and "mythical". What we do factually know today - is very detailed tracking in Iceland and Israel, who were also very PRO-VACCINE. Vaccinating ~90% of their populations, only to see a far worse spike of cases in SARS2 outbreaks that appeared in July August 2021. The inventor of the new mRNA vaccine publicized problems with using the vaccine, warning of manipulating antibodies that would results in weaker SARS2 variants become more virulent and slipping past the VAX'd immune system, creating a huge rebound of illness. And this summer, we are witnessing his expert analysis come to fruition.

On 2020-04-14 01:27:03, user Sinai Immunol Review Project wrote:

Title: Association of BCG vaccination policy with prevalence and mortality of<br /> COVID-19

Immunology Keywords<br /> Bacillus Calmette–Guérin (BCG) Immunization, COVID-19 prevalence, COVID-19 deaths

Main findings<br /> Previously reported immunization programs using BCG vaccines have demonstrated heterologous protection against other unrelated pathogens that associated with lower mortality and morbidity risks [1]. Therefore this study investigated the possible correlation between COVID-19 death cases or prevalence with BCG vaccination. The authors used publicly available COVID-19 data from 136 countries as well as vaccination demographics from the BCG World Atlas to perform a linear regression modeling.

After correcting for life expectancy and the onset of the spread of the virus (n=40), the analyses revealed a positive effect of current BCG vaccination programs and controlling the number of COVID-19 cases and deaths.

The amount of variance explained by BCG vaccination was 20% for number of cases and significant for both groups of countries, the ones that used to have a BCG immunization program in the past (b = 0.6122, p = .0024) and the ones that never have it (b = 0.6511, p = .0326).

Only the group of countries that never vaccinated against BCG showed significance in deaths/cases ratio but explains only 3.39% of the observed variance.

The authors concluded that BCG immunization may provide protection against COVID-19 probably due to the infection spread reduction. BCG immunization doesn’t have a significant impact in the mortality induced by COVID-19.

Limitations:<br /> As acknowledged by the authors of this study, there are large number of unexplained potential confounding variables such as BCG immunization coverage, and onset of virus spread in different countries. <br /> The authors cite that BCG immunization coverage could be variable among countries, but they didn’t explore it. Further, vaccination coverage changes at different rates over time across countries for different reasons [2]. Additionally, the authors did not consider the variable immunization coverage within countries, where unequal access to healthcare is frequently observed [3, 4]. <br /> The authors do not adequately control for time of spread in infection for each country [5].

The authors discuss the importance of validating experimentally the results observed and claim that BCG vaccination could provide non-specific protection against COVID-19. A stronger discussion of the use of BCG vaccine would have included known considerations on efficacy considering route of administration (intravenous, intradermal), vaccine strains which are known to differ in the number of viable bacteria and duration of protection.

Relevance: <br /> This study presented preliminary data on possible non-specific protection by BCG immunization on COVID-19 infection.

References

1. Aaby, P., T.R. Kollmann, and C.S. Benn, Nonspecific effects of neonatal and infant vaccination: public-health, immunological and conceptual challenges. Nat Immunol, 2014. 15(10): p. 895-9.
2. Nuffieldtrust. Vaccination coverage for children and mothers. 2020 [cited 2020; Available from: https://www.nuffieldtrust.o....
3. WHO. 10 facts on health inequities and their causes. 2017; Available from: https://www.who.int/feature....
4. Balance. Health Care Inequality in America. 2020; Available from: https://www.thebalance.com/....
5. Statista. Rate of coronavirus (COVID-19) tests performed in select countries worldwide as of April 8, 2020 (per thousand population)*. 2020; Available from: https://www.statista.com/st....

Review 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 2020-05-06 06:53:53, user Hossein Mirzaei wrote:

Dear Georg<br /> i cant find table 1 in your article, Which you refereed to that for Main characteristics of patient.<br /> can you help me to find that?<br /> Thanks<br /> Hossein

On 2023-11-12 16:14:24, user Julian Gough wrote:

We have noted that in a small number of cases this work is being cited in the literature as a positive GWAS association for the ERAP2 gene, however we would like to be clear that we are making no such claim, and urge authors to take care in citing this work. We are pleased that for the majority of citations authors have not misrepresented the findings.

Analysis of subsequent genetic datasets for COVID-19 mortality [not yet published] could suggest that risk factors (reported here and elsewhere) are different at different points in time, as the virus itself has mutated, medical care has evolved, vaccination has been introduced and population vulnerability and exposure has changed. Therefore we also ask readers to take note that the conditions under which the (very early) data collected by UKbiobank during the first wave of the pandemic -- analysed in this work -- may be very different from present, future or past conditions during other waves of infection.

On 2020-04-22 12:20:25, user Patrick Langer wrote:

Chloroquinederivatives are highly likely to kill male, black patients, because a lot of them have Glucose-6-phosphate-dehydrogenase-deficits so it will cause hemolysis. It's a common fact and I don't get why it is still not widely discussed. Same with people or people with ancestry from other (previous) malaria-endemic areas like Brazil, Ecuador, northern Italy...

On 2020-04-22 00:53:03, user Mike Cee wrote:

This paper is flawed and should be withdrawn immediately.<br /> 1) This paper is flawed due to the limitation discussed on page 12 about the likelihood that the HCQ group, "However, hydroxychloroquine, with or without azithromycin, was more likely to be prescribed to patients with more severe disease, as assessed by baseline ventilatory status and metabolic and hematologic parameters."<br /> Doctors working the front lines have already noted that patients at SYMPTOMS ONSET + 14 days should not be prescribed HCQ<br /> 2) The important grouping by number of days since SYMPTOM ONSET was left out of this study. Previous studies, while anecdotal, suggest that patients should be prescribed HCQ early because it is believed to prevent the virus from infecting the type 2 lung cell through the ACE2 receptor and thus stops the progression of the disease.<br /> 3) This study did not document the dosage given to the patients. That would have been a helpful inclusion so we could understand if the patients who died were actually poisoned by excessive the treatment.<br /> 4) HCQ prescribed in patients in the first week after SYMPTOMS ONSET to include a zinc supplement which anecdotal evidence suggests a dual function of the combination: The HCQ provides an avenue for the zinc to enter the Type 2 lung cell where it interferes with the virus replication process.

On 2020-04-22 20:27:36, user Cannot Write wrote:

The risk is still higher with HC+AZ but the number of patients is too

small, therefore statistically not robust

On 2020-04-22 03:27:17, user Bob Joy wrote:

NY Doctor Treats 699 covid Cases With 100% Success , zinc included

https://everlast.mercola.co...

On 2025-05-21 23:31:22, user Yanning Liu wrote:

This article has recently been published on Radiology https://doi.org/10.1148/radiol.241597

On 2021-12-02 13:00:06, user Jörg Hennemann wrote:

I don`t get the way the data are aquired. The outhers are always refering to "symptomatic infections" and calculate frome those the pandemic development? Including the just positiv tested people without any symptoms? As valid base for modelling such things the real(!) distribution of all (with or without symptoms) infected people or at least those data gotten from a representative cohort of German people has to be used. Those data are not available. I also do not understand the conclusion. If the contribiution to R is 67-76% for unvaccinated and 38-51% of the vaccinated, why i targeted NPIs for the unvaccinated the only solution? How about targeted NPIs for the vaccinated? From a scientific point of view this is an important question that should be answered in your discussion - especially because of the unknown amount if virus carrying vaccinated people. If I had to do the peer review, I had substential questions to be answered befor publishing this...

On 2021-12-02 21:55:33, user Volker wrote:

The main message taken from this "paper" is "we estimate that unvaccinated individuals are involved in 8–9 out of 10 new infections.". This message is as wrong as it seems to be in comparison with the real world.<br /> One must add "that vaccinated individuals are involved in 5–6 out of 10 new infections.", which means "in more than half of new infections vaccinated individuals are involved". This is exactly what is shown in the graphics, too. <br /> The most dangerous thing about this paper is, that it is used as a base for political decisions only in a single part, not in complete.

On 2021-12-01 13:58:36, user Nudnik_de wrote:

I'm missing one parameter in the study. It seems there is no differentiation made under which condition people interact with each other. In other words, whats the impact of 3G and 2G rules? Vaccinated but not tested people meet Unvaccinated but tested folks... I'm concerned that the lack of considering such aspects could have a severe impact on the results and therefor lead to improper measures.

On 2020-04-22 18:28:14, user Clarissa Damaso wrote:

Hi, I'd like to know how you determined virus titter in order to calculate the MOI. It's not in Material and Methods. I'd also like to know why you opted to detect virus RNA during infection instead of checking the production of infectious particles. Thanks.

On 2020-05-25 16:35:51, user HT wrote:

By 24 May, the daily cases crossed 7000, and all projections have gone haywire.

On 2025-03-05 11:17:40, user Eva van Heese wrote:

The peer-reviewed version of this manuscript is now published at: https://onlinelibrary.wiley.com/doi/full/10.1111/jsr.14479

On 2020-08-24 14:30:47, user Javeria wrote:

This will definitely help everyone out until we find out an ultimate treatment. Brilliant work done by the authors!!

On 2025-11-11 03:13:33, user Evolutionary Health Group wrote:

We at the Evolutionary Health Group ( https://evoheal.github.io/) "https://evoheal.github.io/)") really enjoyed this paper.

Here are our highlights:

Triangulating national surveys and HIV self testing kit-distribution data (2012–2024) from 27 African countries, the authors use a hierarchical Bayesian model to estimate adult HIV self-testing uptake by sex/age, map country & regional differences, and infer the share of distributed kits used and re-testing rates.

Uptake is rising: From <1% in 2012 to 6.8% in 2024 overall; men slightly higher than women, and 25–34 year-olds have the highest uptake.

Big regional & country gaps: Eastern/Southern Africa 10.2% vs Western/Central 2.0% in 2024; country peaks reach ~45% in Lesotho.

An estimated ~70% of distributed HIV self testing kits are actually used, and prior users are only slightly more likely to self-test again (RR ? 1.1).

In a serostatus-stratified meta-analysis, people living with HIV not on ART had lower odds of having ever used HIVST (OR 0.75; 95% CI 0.53–1.08), with heterogeneity across countries (e.g., higher odds in Kenya).

On 2020-03-22 10:37:56, user Nathan wrote:

Here's a re-analysis based on mixed-effects logistic regressions, including time and age as covariates: https://nfaivre.netlify.com...

On 2021-09-29 05:55:21, user Maria Schilling wrote:

"Overall, our study demonstrates the potential of mRNA vaccines to induce, maintain, and shape T cell memory through vaccination and revaccination." ????

On 2021-07-06 10:46:11, user Ravi P wrote:

Asymptomatic efficacy of 60% by PCR Testing, Great Find

On 2021-07-04 05:23:23, user PriyankaPulla wrote:

Major protocol violations occurred at the largest site of the Covaxin phase 3 trial, a private hospital called People's Hospital, which recruited 1700 participants. These violations are documented extensively by multiple media outlets. And these violations raise questions about the integrity of the Phase 3 trial data. They also raise questions about the sponsors' attitude to due process, and the independence/training of the DSMB: both sponsors (the Indian Council of Medical Research and Bharat Biotech) responded to the allegations with cursory dismissals, while the DSMB remained mum.

Further details here: https://www.thequint.com/co...

I am listing a few of the documented irregularities:

1. Participants told media outlets that they didn't give their informed consent, an Indian legal requirement. Many participants belonged to disadvantaged tribal communities/were illiterate, which necessitates special consent protocols under Indian law, which investigators didn't follow.

Investigators admitted in a video-recorded press conference that they didn't give participants a copy of their informed-consent form during their first visit, unless participants explicitly asked for it. This strongly suggests that the investigators weren't trained in Indian legal requirements or Good Clinical Practices.

1. Investigators allegedly advertised the trial as a vaccination drive in communities of poor and illiterate people.

2. Dozens of participants say the trial team did not contact them to record solicited adverse events. These participants often didn't have their own mobile phones (mobile phones are the mode through which solicited adverse events were to be collected, as per trial protocol). Even though these participants came from poor communities, investigators didn't foresee the fact that they may not have their own mobile phones, and may be hard to contact. Nor did they attempt to contact them in their homes in the days following the doses.

3. People's Hospital recruited a record 1700 participants in 1.5 months (no other Covaxin trial site in India managed such numbers). In contrast, another government-run Covaxin site in Bhopal struggled to even recruit a few hundred participants, and was, therefore, excluded from the trial. This supports the allegation that People's Hospital misadvertised the trial as a vaccination drive.

4. Many participants told media outlets that they suffered Covid-like symptoms post jab, but the investigators never called them to collect this information. Nor did the participants know where to report their symptoms. This raises questions about how well Covid cases were recorded.

5. Participants say they were denied medical treatment at People's Hospital when they fell sick. This, again, raises questions about how well the investigators captured adverse-events.

6. When one participant at the Bhopal site died, investigators ignored his family's version of the participant's symptoms in their causality analysis. In the family's version, the participant suffered from very severe symptoms (vomiting, dizziness, weakness) for 7-8 days before death, while the investigators claimed he was fine during solicited-adverse event monitoring, and died suddenly.

The dismissal of the family's version of events, when the family was present during the participant's death (but the investigators weren't), raises serious questions about how Serious Adverse Events are investigated. No post-mortem report or causality analysis was shared with the family despite multiple requests. Further, the family alleges that the deceased participant received no phone calls from the investigators to record solicited adverse events in the days leading up to his death.

The investigators could easily have shared proof of their claims by sharing a record of the phone calls with the family. They haven't.

Despite the above serious concerns (which are supported by video testimony from participants broadcast on multiple media outlets, specifically NDTV), the trial's government sponsor, ICMR, and Bharat Biotech, denied all allegations in a cursory manner. Further, the preprint makes no mention of them, or explain how these irregularities were handled.

This raises questions about overall data integrity in Bharat Biotech's phase 3 trial. Bharat Biotech has been under substantial pressure from the government to roll out Covaxin fast, which may explain why the company is overlooking such data integrity issues. More details here: https://www.livemint.com/sc...

Reviewers of this paper, and licensing authorities, including the World Health Organisation, must investigate these allegations thoroughly.

On 2025-07-01 21:10:32, user Abraham Keffale Keffale Mengis wrote:

please add the published version it is published in scientific reports https://doi.org/10.1038/s41598-025-08005-2

On 2021-09-10 07:18:16, user Michael Gardner wrote:

JimmyJoe6000, I have the same question. If you, or anyone else, has the answer please post it.

On 2020-07-05 14:07:29, user mike marchywka wrote:

I noted my comments on twitter re this paper were piciked up here. You can see it referenced in context here, fwiw, <br /> https://www.linkedin.com/po...

On 2020-04-23 21:11:29, user Paul Arveson wrote:

Do you need a sterile swab or just a Q-tip?

On 2020-07-27 19:13:51, user Leah McElhanon wrote:

We are currently using saliva specimens to detect SARS-CoV-2. Do you have any additional data are resources we can take a look at? Thanks in advance.

On 2020-06-30 12:50:48, user Dude Dujmovic wrote:

"Secondary cases"? I think you need to precisely define what do you mean by that. The whole paper is extremely vague in what the numbers are about.

On 2021-08-13 10:22:44, user Javier Mira wrote:

Correlation doesn't mean causality. One can't infere any conclusion from just a correlation between 2 variables because there can be higher order variables governing those 2. If we made that we could conclude that bringing storks to our village would help increase the population growth rate, which is obviously false.

On 2021-10-06 17:34:27, user zega wrote:

Problem in the study is you include only "patients" and work from there, asymptomatic rate for 19yo can be found in https://www.nejm.org/doi/fu... and is 94-90% over time where it settles@90% cumulative and positivity rate 0.8%/1wk 2.1%/wk2 2.7%/wk3/-cumulative where rate of change slows and flatline. Vaccine is ment to be administered to everyone, in that case harm proportion difference is vast, so in case you closely monitor infection you will catch way more cases that changes the harm ratio outcome.

On 2022-10-24 11:51:28, user Indi Trehan wrote:

This article has now been published after peer review: The Journal of Pediatrics 2022; 247: 147-149. doi: 10.1016/j.jpeds.2022.05.006.

On 2021-01-07 14:34:51, user Meerwind7 wrote:

Households with single parents are also considered as socially deprived in other contexts. For infection rates, it might be of benefit if there is no second adult that could bring infections to the family. It was a pity if the effect was not taken into account. I also do not know if the social deprivation was evaluated for each individual child and its infection risks, or just for the schools and the aggregat of their pupils overall.

On 2020-08-17 22:56:26, user Irene Tosetti wrote:

identical to the French test (already for sale in Europe) called Easycov, a saliva rt-lamp. Good job.

On 2023-01-13 11:35:49, user SB wrote:

Hi, thanks for the preprint.<br /> I do not understand the last sentence of the conclusion "Individuals with hybrid immunity had the highest magnitude and durability of protection against all outcomes". That's because the results section pointed out: "Against reinfection at 6 months, there was similar protection from HE with first booster vaccination (effectiveness 46·5% [36·0-57·3%]), HE with primary series (60·4% [49·6-70·3%]), and prior infection alone (51·2% [38·6-63·7%]), with all three types of immunity conferring significantly greater protection than primary series vaccination alone (15·1% [11·3-19·8%]) or first booster vaccination alone (24·8% [18·5-32·5%])"<br /> So the protection against reinfections seems to be for hybrid immunity NOT OVER then for other types of immunity.

On 2025-04-23 12:00:02, user Pei Meng wrote:

I read your paper with great interest, but I have a question regarding the following statement:

“This approach identified putative drivers for all aut-mCAs (Table 1). Annotation of driver genes as tumor suppressors or proto-oncogenes revealed that every + aut-mCA contained proto-oncogenes as putative drivers, notably every – aut-mCA contained tumor-suppressors as putative drivers, and = aut-mCAs contained either proto-oncogenes and tumor-suppressor drivers.”

I noticed that TP53 is located on chromosome 17p, and from Extended Figure 2, there appear to be some losses on chromosome 17q. These 17q losses don't seem to contain tumor suppressors as putative drivers. Could you please clarify how these cases were classified, and whether 17q losses were considered as – aut-mCAs without tumor-suppressor drivers?

On 2021-10-12 07:42:23, user Ralph Feltens wrote:

One conclusion that can not be drawn from this study is that vaccination (with a mRNA-based Covid-19 Vaccine) provides stronger immunity than a SARS-CoV-2 infection.<br /> In contrast to an infection with the virus, with the mRNA-based vaccine only antibodies against the spike protein are produced.

And T- and B-cell-based immunity is another topic altogether ...

On 2020-08-24 08:15:32, user Mark Wilson wrote:

A weak surrogate end point (droplets). Speak to surgeons about masks and they tell a different story. https://fee.org/articles/eu...

On 2021-10-10 05:14:46, user kdrl nakle wrote:

Needs to point out that this is all prior to Delta and that changes everything.

On 2021-10-21 01:57:10, user Sook Wah Yee wrote:

Great work @Eric_Fauman: I am so excited but I did not see that Supplemental Tables are attached with this paper? Or did I miss it? I only see one pdf file attached with Supplemental Figures. Thanks for checking.

On 2024-12-23 02:34:26, user IA Signore wrote:

Now published as Signore, I. A., Donoso, G., Bocchieri, P., Tobar-Calfucoy, E. A., Yáñez, C. E., Carvajal-Silva, L., ... & Colombo, A. (2024). The Chilean COVID-19 Genomics Network Biorepository: A Resource for Multi-Omics Studies of COVID-19 and Long COVID in a Latin American Population. Genes, 15(11), 1352.

On 2021-08-01 12:27:54, user Oscar Perez wrote:

Table S4 shows 32 deaths among the vaccinated. 33 among the placebo. The vaccine is safe and effective. ????????????

On 2021-07-29 15:40:59, user Peter P.V wrote:

Every six month new vaccine will have to be developed. Is it possible?

On 2022-11-10 09:21:51, user Clive Bates wrote:

Please see our post-publication peer review of this pre-print published at Qeios.

Bates, C., Youdan, B., Bonita, R., Laking, G., Sweanor, D., & Beaglehole, R. (2022). Review of: “Tobacco endgame intervention impacts on health gains and Maori:non-Maori health inequity: a simulation study of the Aotearoa-New Zealand Tobacco Action Plan.” Qeios DOI 10.32388/8WXH0J

The paper, Ouakrim et al., refers to modelling of proposed New Zealand legislation that would make deep reductions in the nicotine in cigarettes. The review notes that the authors have assumed this will lead to an 85% reduction in smoking over five years, with almost one-third of smokers quitting in each year. Our Qeios review examines the origins and credibility of that assumption.

We identify ten flaws in the modelling and stress that the smoking cessation trial on which its assumptions are largely based is not a viable proxy for assessing the impact of a market-wide regulatory intervention. The modelling does not simulate the most likely behavioural responses that would follow from such an intervention and does not address plausible unintended consequences such as illicit trade, hoarding or workarounds..

I should stress that this review of the modelling is not intended as a decisive argument against the proposed denicotinisation policy. It is, however, an argument against relying on this modelling to justify the policy. There are other considerations both for and against the policy.

Our review should be seen as a constructive contribution to sound policy-making. Decision makers should should proceed without over-reliance on modelling, knowing its limitations, possible risks and likely unintended consequences. The reveiw authors have not explicitly opposed the measure but suggested it needs to be re-evaluated: <br /> (1) with a deeper assessment of the risks of unintended consequences; <br /> (2) against a maximalist approach to voluntary tobacco harm reduction as the counterfactual (not just business as usual); <br /> (3) a better understanding of how it will work for the most disadvantaged people and communities.

On 2022-01-31 18:32:19, user Jared Roach wrote:

These are very minor comments about the wording of the Abstract that I would make if I was reviewing the paper:

"strikingly different"<br /> I would delete the vague adjective "strikingly" as it could be interpreted many different ways. Rather insert the exact number of mutations or some similar quantitative metric.

"rapidly replaced"<br /> maybe OK to leave "rapidly", but also add in a sense of how long (e.g., over a period of 3.5 weeks) - or whatever the number of weeks was.<br /> "rapidly" makes sense only in context of other strain replacements such as Alpha-> Delta or Delta-> Omicron. If it isn't much faster than these, I would use an exact time rather than the comparative and vague adjective "rapidly"

On 2020-06-13 21:16:27, user John Liang wrote:

I think the theory of urns estimate is highly inaccurate for a lot of reasons, it is highly unscientific and a lot of guess work. I will list a few points here

1. Cremation service requirement in Wuhan is always around 28-2900 every six months this is before the addition of CVOID related death and can be found .

2. You did your guest work about urns number base on urns order by '1' cremation service company and there were no observation at other 7 cremation service companies. There is no confirmation of the other 7 actually order that many urns, how frequent the urns were ordered during the period? Was the urns ordered was a preparation for the future 6 months or 3 months?

3. Each cremation service companies have different service capability it is unscientific to assume all 8 would be order the same number of urns.

4.The time take for a complete cremation service is around 3-4 hours not 2 hours.

On 2021-08-11 14:46:17, user Richard Bruce wrote:

This is a very informative study. The methods do not say how testing for infection was handled to ensure uniformity of testing frequency between the different cohorts. Given the retrospective nature, there may be a selection bias. If we assume that vaccination reduces symptoms (which is reasonable given many data points including this paper), we can also then assume that subjects will seek testing more frequently when symptoms are present than in the absence of symptoms. Therefore, given that unvaccinated will be more likely to experience symptoms following infection, unvaccinated subjects are more likely to receive testing when infected. This will bias the infection rates but should leave the hospitalization/ICU rates unchanged.

On 2024-07-15 22:25:43, user Ashraf Fawzy wrote:

A peer reviewed version of this article has been published in the American Journal of Respiratory and Critical Care Medicine: https://www.atsjournals.org/doi/abs/10.1164/rccm.202401-0036LE

On 2021-09-22 12:36:03, user Jakefromstatefarm wrote:

So if the myocarditis rate is 1/1000 and nearly all of those that developed it were men, isn't the real number for men more around 1/500?

On 2020-04-06 12:25:59, user Sinai Immunol Review Project wrote:

Clinical Characteristics of 2019 Novel Infected Coronavirus Pneumonia:A Systemic Review and Meta-analysis

The authors performed a meta analysis of literature on clinical, laboratory and radiologic characteristics of patients presenting with pneumonia related to SARSCoV2 infection, published up to Feb 6 2020. They found that symptoms that were mostly consistent among studies were sore throat, headache, diarrhea and rhinorrhea. Fever, cough, malaise and muscle pain were highly variable across studies. Leukopenia (mostly lymphocytopenia) and increased white blood cells were highly variable across studies. They identified three most common patterns seen on CT scan, but there was high variability across studies. Consistently across the studies examined, the authors found that about 75% of patients need supplemental oxygen therapy, about 23% mechanical ventilation and about 5% extracorporeal membrane oxygenation (ECMO). The authors calculated a staggering pooled mortality incidence of 78% for these patients.

Critical analysis:<br /> The authors mention that the total number of studies included in this meta analysis is nine, however they also mentioned that only three studies reported individual patient data. It is overall unclear how many patients in total were included in their analysis. This is mostly relevant as they reported an incredibly high mortality (78%) and mention an absolute number of deaths of 26 cases overall. It is not clear from their report how the mortality rate was calculated. The data is based on reports from China and mostly from the Wuhan area, which somewhat limits the overall generalizability and applicability of these results.

Importance and relevance: This meta analysis offers some important data for clinicians to refer to when dealing with patients with COVID-19 and specifically with pneumonia. It is very helpful to set expectations about the course of the disease.

Francesca Cossarini

On 2020-06-18 12:17:43, user Paul Warren wrote:

the discussion states that: ‘There are three types of risk for medical staff. The first relates to their biology, the second their environment and the third to the exposure. This tool evaluates the former in order to advise mitigation of the latter...’ Leaving aside the clumsy english, as I understand it the tool is evaluating data on covid deaths from ICNARC. To die from covid you have to catch it and then fall ill, so it is a composite measure of exposure, biological factors, and other bits and pieces – health behaviors and so on. How this composite cashes out is generally thought to depend on the risk factor in question. For<br /> instance the risk of increasing age may be more to do with biology than exposure, whereas for ethnicity many commentators say that exposure probably is an important factor. So, to a variable extent, the tool uses a measure of exposure across society as a whole to advise on exposure mitigation in healthcare settings. Now in practice this may not be a great problem, but isn’t it at least worth a mention?<br /> Hardly a concern, maybe just something as a nonscientist I struggled with was relative<br /> and absolute risk. Does normalising the risks to 40-49yr old women have any effect on the relative scores of the different risk factors, when compared with other possible choices, say 20-29yr women or whatever? My logic isn’t up to it, but if it does make a difference the choice of 40-49 would need justification. Also, does the correlation with opensafely and PHE document absolute risk scores mean that this tool could be used to judge absolute risk? While for justice and equity relative risk may be the best measure, in other situations both employer and employee may want some idea of absolute risk.

On 2020-08-08 22:41:29, user Erhannis Kirran wrote:

Spelling error, Line 55, "Covit-19"

On 2020-04-01 13:40:40, user Sinai Immunol Review Project wrote:

Title: Correlation between universal BCG vaccination policy and reduced morbidity and mortality for COVID-19: an epidemiological study

Keywords: BCG vaccine – epidemiology – vaccination policy

Main findings:The authors compared middle and high income countries that never had a universal BCG vaccination policy (Italy, Lebanon, Nederland, Belgium) and countries with a current policy (low income countries were excluded from the analysis as their number of cases and deaths might be underreported for the moment). Countries that never implement BCG vaccination have a higher mortality rate than countries which have a BCG vaccination policy (16.38 deaths per million people vs 0.78). Next, the authors show that an earlier start of vaccination correlates with a lower number of deaths per million inhabitants. They interpret this as the vaccine protecting a larger fraction of elderly people, which are usually more affected by COVID-19. Moreover, higher number of COVID-19 cases were presented in countries that never implemented a universal BCG vaccination policy.

Limitations:While this study aims to test an intriguing hypothesis unfortunately, the data is not sufficient at this time to accurately make any determinations. Several caveats must be noted including: not all countries are in the same stage of the pandemic, the number of cases/deaths is still changing very rapidly in a lot of countries and thus the association may only reflect exposure to the virus. This analysis would need to be re-evaluated when all the countries are passed the pandemic and more accurate numbers are available. Additionally, very few middle and high-income countries ever implemented universal BCG vaccination, which can be a source of bias (5 countries, vs 55 that have a BCG vaccine policy). Effective screening and social isolation policies also varied considerable across the countries tested and may reflect another important confounder. The authors could consider analyzing the Case Fatality Rate (CFR, % of patients with COVID-19 that die), to more correct for exposure although testing availability will still bias this result. Variability in mortality within countries or cities with variable vaccination and similar exposure could also be appropriate although confounders will still be present.

Relevance:BCG vaccine is a live attenuated strain derived from Mycobacterium bovis and used for a vaccine for tuberculosis (TB). This vaccine has been proven to be efficient in preventing childhood meningitis TB, but doesn’t prevent adult TB as efficiently. For this reason, several countries are now only recommending this vaccine for at-risk population only.<br /> This study shows that there is a correlation between BCG vaccination policy and reduced mortality for Covid-19. Indeed, BCG vaccine has been shown to protect against several viruses and enhance innate immunity1, which could explain why it could protect against SARS-CoV-2 infection, but the exact mechanism is still unknown. Moreover, the efficiency of adult/older people vaccination and protection against Covid-19 still needs to be assessed. Regarding this, Australian researchers are starting a clinical trial of BCG vaccine for healthcare workers2, to assess if it can protect them against Covid-19.

1. Moorlag SJCFM, Arts RJW, van Crevel R, Netea MG. Non-specific effects of BCG vaccine on viral infections. Clinical Microbiology and Infection. 2019;25(12):1473-1478. doi:10.1016/j.cmi.2019.04.020
2. BCG vaccination to Reduce the impact of COVID-19 in Australian healthcare workers following Coronavirus Exposure (BRACE) Trial | Murdoch Children’s Research Institute. https://www.mcri.edu.au/BRACE. Accessed March 31, 2020.

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

On 2020-04-04 22:05:26, user PhilipandHeidi Kapitaniuk wrote:

Here in France the BCG has been widely used, and we still are losing many people to the Coronavirus. They need to be looking at more than just a few countries. This does not sound serious to me.

On 2020-03-29 23:18:26, user MVianna wrote:

This is quite interesting. I was wondering, however, if you have taken into consideration the onset date of the infection in each country. Because when you consider the number of deaths per mi habitant you may be comparing data from countries with different stages of the contamination. It seems that lower income countries are going to be affected later in time and this could significantly impact the effect you observed in Figure 1.

On 2020-04-05 10:52:14, user Charlie Massey wrote:

Do you perhaps have a link to his publication? - Would love to read it!

On 2021-10-23 08:34:43, user Leslie Viljoen wrote:

Is there any way to be notified when a preprint completes peer review?

On 2020-04-04 18:33:11, user Jhansi Dan wrote:

Do anyone have data from last saturday/sunday for Virginia state. I remember seeing the peak date as April 28th and it shows May 20 now. I deduce flattening of curve. Please share the graphs. I wish they have archives for past data to compare.<br /> Thank You

On 2020-09-28 09:44:58, user markd wrote:

• very low copies number for air samples, would like to know the LOD for the detection method(s)
• 300l/' x 10' = 3mc, 50l/' x 10' = 0.5mc - why didn't you keep analysis volume the same across sites/samplers?
• can you report on the state/condition of ventilation in the sampled rooms?

On 2020-05-11 10:58:14, user Paul Revere wrote:

https://www.cdc.gov/nchs/nv...

Here is the CDC data. Approximately 20,00 excess deaths in April in NY area mainly but overall US deaths YTD below three year average.

On 2020-04-03 03:05:56, user Philomena Okeke wrote:

I like more studies and research to be done on this.If group A+ are vulnerable then they should be protected from this Coronavirus.The B and O should really help especially the 0 group. I am sure that more researchers need to provide more evidence on this critical issues. <br /> Thanks

On 2021-05-28 08:48:55, user Enzo wrote:

Yet another huge double mistake :<br /> In Fig.6 (viral clearance) for Karamat study, the number of events are WRONG, and they're represented on the WRONG SIDE. <br /> Karamat counts nb of viral clearance at day 3 (17 IVM vs 2 control), then the *additional* number at day 7 (20 more in IVM group vs 18 more in control group). Fig.6 only counts the additional count between day 3 and day 7, and forgets what happened till day 3. <br /> Hence the figures in Fig.6 for Karamat should be either "17 for Ivermectin and 2 for Control" or "37 for Ivermectin and 20 for Control". <br /> And these figures are IN FAVOR of ivermectin. Even the wrong "20" and "18" should have been represented on the "favors IVM " side.

On 2020-07-23 11:59:38, user Mr C S Mence wrote:

All the researchers seem to be north of the equator. Is there any data from countries south of the equator who have experience of the pandemic through their winter months

On 2021-12-04 08:24:25, user Benjamin George wrote:

I am skeptical about a paper that was designed with the alpha and delta variants in mind and reinfection rates. <br /> How does a paper that reviewed data from March 2020 to November 27 2021, suddenly include with great conviction that Omicron picked up on Nov 16 and 17 samples and announced on November 25 as a new variant show higher reinfection rates. <br /> All based on a few days of studies. <br /> And Omicron dropped into the summary to add credibility to the paper!

One should question the validity and professionalism of the writers.

On 2020-04-07 18:16:27, user xahdum16x wrote:

This study at this time is useless to me. What is the comorbid breakdown of the patients, they only say sex and age are homogenous. What is the CI of the results, I don't care about a low pvalue. What were the "moderate adverse reactions" and how did they judge pneumonia improvement on imaging, what category since all these patients were mild to moderate where there baseline imaging similar or not. Lastly, since it does not say blinded, maybe the physicians were more apt to hold off on aggressive therapy in the "treatment" arm as opposed to the "placebo arm" due to flase security or hoping that it would help create significant results. There is a reason we blind studies to prevent bias.

On 2020-05-07 00:09:49, user Charles Warden wrote:

I think I saw something roughly similar in this Tweet:

https://twitter.com/manuelr...

However, I have the following questions:

1) How are you taking into consideration lack of exposure? If you looked for a difference in prognosis among infected individuals, then that would provide a control that you know all individuals have been exposed to the virus. I realize this may not be exactly what you are looking for, but I would expect a small proportion of individuals having been exposed to the virus will make achieving significance for infected versus uninfected individuals more difficult.

2) If you had antibody results, maybe this would help (even if that is also not perfect), but my understanding is that you are also not using that as a filter (which I am guessing is not available)?

3) It looks like you considered Exome data. I think that this may be good because I would have guessed you might miss a signal with SNP chip data, if the relevant variants are not common (or at least not well characterized as part of larger haplotypes). However, is it possible that variant calling for most genes is less optimal with these genes? Is there any way to go back to the raw data and see if the variant calling strategy can change anything among infected individuals?

4) If all of the above criteria are meet, do you need to consider non-genetic risk factors (such as age) into your model?

5) A lack of a significant result is not the same as saying with high confidence that a hypothesis cannot be true. I think that you should communicate what you have observed in some way, but I think some caution might be needed to avoid confusion. For example, a reader from the general public might think you are confident that you have found results that contradict reports that ACE2 (and/or TMPRSS2) may be important for COVID-19 infections. My guess is this is not what you meant, but I wonder if the limitations to these results need to be emphasized more.

If this provides me a way to ask these questions in a way that gets less attention from the general public, then I think it is good that you posted these results. Discussion about possible implications could be important, but my understanding is that this does not mean that this is strong evidence that the current public health recommendations should be changed (and I don’t want to cause any unnecessary confusion).

On 2020-06-08 21:16:33, user Christian Lehmann wrote:

nice article - the problem is the communication in by the public media - The authors show a ASSOCIATION - this is something completely different from a causality - so please be careful, having a certain blood group does not tell you something about your possible disease outcome.

On 2020-03-24 04:17:55, user Sinai Immunol Review Project wrote:

Main findings<br /> The authors performed single-cell RNA sequencing (scRNAseq) of peripheral blood mononuclear cells isolated from whole blood samples of COVID-19 patients (n=10). Data was compared to scRNAseq of samples collected from patients with influenza A (n=1), acute pharyngitis (n=1), and cerebral infarction (n=1), as well as, three healthy controls. COVID-19 patients were categorized into those with moderate (n=6), severe (n=1), critical (n=1), and cured (n=2) disease. Analysis across all COVID-19 disease levels revealed 56 different cellular subtypes, among 17 immune cell types; comparisons between each category to the normal controls revealed increased proportions of CD1c+ dendritic cells, CD8+ CTLs, and plasmacytoid dendritic cells and a decrease in proportions of B cells and CD4+ T cells.

TCR sequencing revealed that greater clonality is associated with milder COVID-19 disease; BCR sequencing revealed that COVID-19 patients have circulating antibodies against known viral antigens, including EBV, HIV, influenza A, and other RNA viruses. This may suggest that the immune response to SARS-CoV-2 infection elicits production of antibodies against known RNA viruses.

Excluding enriched pathways shared by COVID-19 patients and patients with other conditions (influenza A, acute pharyngitis, and cerebral infarction), the authors identified the interferon-MAPK signaling pathway as a major response to SARS-CoV-2 infection. The authors performed quantitative real-time reverse transcriptase polymerase chain reaction (RT-PCR) for interferon-MAPK signaling genes: IRF27, BST2, and FOS. These samples were collected from a separate cohort of COVID-19 patients (critical, n=3; severe, n=3; moderate, n=19; mild, n=3; and cured, n=10; and healthy controls, n=5). Notably, consistent with the original scRNAseq data, FOS showed up-regulation in COVID-19 patients and down-regulation in cured patients. The authors propose that FOS may be a candidate marker gene for curative COVID-19 disease.

Limitations<br /> The sample size of this study is limited. To further delineate differences in the immune profile of peripheral blood of COVID-19 patients, a greater sample size is needed, and longitudinal samples are needed, as well. A better understanding of the immunological interactions in cured patients, for example, would require a profile before and after improvement.

Moreover, the conclusions drawn from this scRNAseq study point to potential autoimmunity and immune deficiency to distinguish different severities of COVID-19 disease. However, this requires an expanded number of samples and a more robust organization of specific immune cell subtypes that can be compared across different patients. Importantly, this criterion is likely needed to ensure greater specificity in identifying markers for COVID-19 infection and subsequent immune response.

Relevance<br /> At the single-cell level, COVID-19 disease has been characterized in the lung, but a greater understanding of systemic immunological responses is furthered in this study. Type I interferon is an important signaling molecule for the anti-viral response. The identification of the interferon-MAPK signaling pathway and the differential expression of MAPK regulators between patients of differing COVID-19 severity and compared to cured patients may underscore the importance of either immune deficiency or autoimmunity in COVID-19 disease.

On 2021-10-03 09:35:28, user kdrl nakle wrote:

Nothing new in this paper.

On 2020-04-27 18:28:36, user stephen zhang wrote:

Published in Brain Behavior and Immunity

On 2020-03-25 20:57:32, user Sinai Immunol Review Project wrote:

Summary of Findings: <br /> - Study used online datasets (scRNAseq GSE131685, scRNAseq GSE107585, Human Protein Atlas, GTEx portal, CCLE) to analyze ACE2 expression in different human organs. <br /> - Study re-analyzed three clinical datasets (n=6, n=99, and n=41) to show 3~10% of 2019-nCoV patients present with abnormal renal function. <br /> - Results indicate ACE2 highly expressed in renal tubular cells, Leydig cells and seminiferous ductal cells of testis.

Limitations: <br /> - Very preliminary transcript/protein dataset analysis in healthy cohorts; does not necessarily translate to actual viral tropism and permissiveness. <br /> - Clinically, would be important to determine with larger longitudinal dataset if SARS-CoV-2 infection changes sperm quality or testicular inflammation. <br /> - Similarly, would be important to determine if simultaneous HBV or syphilis infection and orchitis impacts SARS-CoV-2 severity. <br /> - Examination and follow-up of renal function and viral orchitis/sperm quality of CoVID-19 patients not done in this preliminary study.

Importance/Relevance: <br /> - Kidney ACE2 result supports other concurrent sequencing studies (https://doi.org/10.1101/202... ) and clinical reports of abnormal renal function or even kidney damage in patients infected with 2019-nCoV (https://doi.org/10.1101/202... ). <br /> - High ACE2 expression in testis suggests potential tropism of the virus to testicular tissues and indicates potential risks for male fertility. Viral orchitis reported for SARS-CoV previously [1], but no clear evidence so far of infertility in SARS, MERS or CoVID-19 patients.

References:

1. Xu, J., et al., Orchitis: a complication of severe acute respiratory syndrome (SARS).Biol Reprod, (2006) 74(2):p 410-6. Doi: 10.1095/biolreprod.105.044776

Review by Samarth Hegde as part of a project by students, postdocs and faculty at the <br /> Immunology Institute of the Icahn school of medicine, Mount Sinai.

On 2020-06-06 01:33:13, user David Hood wrote:

I think the "39.5% of cases seeking medical consultation in primary care settings" may be overly conservative in the model for a parameter representing getting medical advice, as it is based of influenza in the 2018 'flu season (a fairly typical year). We know from the ESR influenza surveillance site that healthline historically (I don't know the period for what they determine historical) get around 40000 Influenza like illness calls a year, and for the period from the week of 14/2 to 29/5 there are historically around 10000 ILI calls. In 2020, for the period from the week of 14/2 to 29/5, there were around 26000 ILI calls. Even allowing for false positive worries from anxious people boosting call numbers, it suggests that people seeking official advice about ILI is dramatically higher in 2020 (which I also acknowledge is not the same as visiting a primary care location about an ILI, which is the 39.5% figure, but the official advice was to ring Healthline, who were presumably advising testing/ isolation/ primary health as appropriate)

On 2020-05-22 01:23:58, user Leonidas Palaiodimos wrote:

This article has been peer-reviewed and published at Metabolism

On 2025-09-13 04:47:02, user Dr. Bügar wrote:

Fascinating. Incredible work!

On 2020-07-07 18:11:59, user Tajemniczy don Pedro wrote:

Makes sense. https://pubmed.ncbi.nlm.nih...

On 2020-04-18 17:22:02, user I.J. Frame wrote:

You rightly point out that your estimates largely depend on the lateral flow test performance, including specificity. To what extent did you (or the test manufacturer) evaluate cross reactivity with serum positive for antibodies against coronaviruses OC43, NL63, 229E, or HKU-1? I think demonstrating that the assay does not cross react with these coronaviruses will help strengthen your work.

On 2020-04-17 21:03:35, user John Ryan wrote:

The researchers identified that 50 out of 3,300 participants tested positive for CV-19 antibodies. Spinning this as 50 to 80 times greater than current prevalence rates as determined through testing is disingenuous. The posted study does not account for the significant upward adjustment from 1.5% of participants to a 2.4% to 4.2% in the general population given the study participants were a skewed convenience sample drawn from Facebook participants, many who believed they had been exposed to CV-19 and had had previously experienced symptoms consistent with CV-19.

On 2020-04-19 05:26:23, user David Feist wrote:

This study has a very high probability of being correct in my opinion, as it is in line with three or four recent seroloprevalence tests (conducted by experts). The Gangelt, Germany test suggested that 15% of the population was infected and that under reporting was of a similar level as that in California.

The high levels of infection explain of course why the pandemic turned down two weeks BEFORE the lockdown in Wuhan, (Wittkowski, MedArxiv, April 2020); herd immunity levels of infection were probably being reached. If there was actually 50 times more cases in Wuhan (ie at least 2.5 million people infected out of a 10 million polualtion) herd immunity may have been reached - if a further 35-30% of residents had cross immunity from prior exposure to cold corona viruses.

The IFR is also now in line with what this study's primary author, John Ioannidis, predicted in the beginning from the Diamond Princess cruise ship data, namely about 0.1%. No Government in the world should have commenced lockdowns based on that February, 2020 data and prediction. Mr Ioannidis should be consulted in the future.

On 2020-04-18 17:13:58, user Animesh Ray wrote:

I do not believe these conclusions. A crucial control for the estimate of false positive detection by their method is grossly inadequate. This manuscript should not have seen the light of the day in this form, let alone be published even in a pre-print format because of the sensitivity of the topic.

Here is the reason: The common cold coronaviruses that could potentially cross-react to existing pre-COVID19 IgM/IgG are quite prevalent in the population. To address this, the authors tested 30 pre-COVID19 sera.

Given an unadjusted detection rate of 2.8% seropositives in post-COVID-19 samples, if all were false positives, they needed to test, for 99% confidence, a MINIMUM of log(0.01)/log(0.972) = 162 pre-COVID19 sera of similar demographics (age/sex/location).

Instead, they tested only 30!

[They do cite the kit validation data by the supplier/vendor as having tested 371 negative samples--this is as spurious an argument as stating that a q.RT-PCR kit produced x frequency of true negatives by the supplier and therefore we don't need to do the appropriate control in our experiment!! This statement has no place in a scientific publication other than trying to obfuscate the real weight of the lack of sufficient control to determine the false positive rates.]

On this basis I cannot attach any value to this report.

These false conclusions, given the current pre-print version, are dangerous because they could be naively interpreted to imply a lesser morbidity of COVID19 than the current numbers otherwise suggest.

I fear that this pre-print will now be used by the public media and sections of political interest groups to advocate for lesser stringency in COVID-19 pandemic control than desirable, and might lead to unfortunate loss of lives.

On 2020-04-24 23:48:17, user endmathabusenow wrote:

The recruitment methods from this study are unbelievable. They include an email that makes inaccurate claims that 1) the FDA approved the test and 2) "In China and U.K. they are asking for proof of immunity before returning to work"

https://old.reddit.com/r/Co...

On 2020-05-13 18:10:56, user João Conrado Blum Júnior wrote:

The finding is reliable. Great text. Congratulations!

On 2021-08-18 18:40:47, user Sumit Rawat wrote:

News article by ET health <br /> https://indianewsrepublic.c...

On 2020-05-26 00:44:57, user Bill Jackson wrote:

It may be related to the amount of virus they faced when there were first infected. In theory one single virion can progress to an infection, but the infective cascade proceeds more slowly in that case and the innate immune system as well as the adaptive immune system are initiated as soon as the initlal infection begins by lysing cells - which may provide a progressively developing immunity that is able to suppress the virus before a fatal case develops. Casual air born infection has the potential to initiate the infection from this small initial exposure. On the other hand, a person, in a seniors home with the air full of particles could get a massive infection of many thousands of virus partcles and the virus cascade from this larger initial infection can increase the circulating load of virus in the blood to lead to the death of many more body cells. In a weaker, older person this might explain the high fatality rates in seniors or others who are in a weakened state.<br /> We do know that places with very high rates of testing, coupled with a high rate of infection tracking and isolation have been able to 'flatten the curve' as they say.<br /> We also know this virus is slower than flu virus in the progression from cell infection to cell death - which gives more time for the innate and adaptive immune systems to quell the infection.

On 2020-05-21 18:45:30, user Political Hack wrote:

One article referencing this paper states: "The U.S. could have prevented roughly 36,000 deaths from COVID-19 if broad social distancing measures had been put in place just one week earlier in March." So what assumptions did the authors use as far as distancing? Did it use our "current" approach or the "early" approach. Basically, did it include use of masks? That is only a recent change to protocol when we go out in public as the early "science" said wearing masks provided no protection. People were still frequenting essential businesses (grocery stores/Home Depot) at the start of the lockdowns and masks we<br /> re a very rare sight. Based upon what we know now regarding transmission mechanisms, there is little doubt that there was rampant spread during lockdowns thanks to the lack of masks. The number of cases kept going up rapidly for MANY WEEKS during the lockdown, surely for this reason. I certainly hope the peer reviewers have the insight to consider that.

On 2021-01-12 19:27:05, user Antonio Bernabe-Ortiz wrote:

A little favor to the authors... please adjust the estimates by ischemic heart disease as there is a potential disbalance between arms as seen in Table 2... thanks...

On 2021-10-13 14:52:47, user Stephen B. Strum wrote:

Everyone has their unique response to an antigen, be it natural or a vaccine. The proof of the pudding is the end response relating to protection--from severe illness, to chronic COVID-19, to hospitalization, to needing an ICU, and to death. For certainty--being vaccinated is better than not. For breakthrough infections the data "appears" that Moderna is superior to Pfizer--but how about an analysis of those who had breakthrough infections? Age, Sex, BMI, Diabetes, Immune status, Medications, etc? I have not read the full paper but going through the publication I do not see that mentioned. How about a probably surrogate or correlate of protection in the form of total immunoglobulin (Ig) G against the S1 protein as measured by the LabCorp or Quest Roche Elecsys test? In my case (age 79, light chain amyloidosis in complete remission (CR) & off chemo or immunotherapy x 1 year) my SARS-CoV-2 Ab (antibody) level at 1 month post two doses of Pfizer was > 250 U/ml, only to drop to 59 at 4 months. Then, I received a Moderna booster on 9/1/21 & on 10/5/21 my Ab level was > 2,500 U/ml. These are tests that are commercially available. The results are back in 24 hrs; the test is not expensive. There's a huge difference in individuals, especially by age and by comorbidity. <br /> LabCorp test code 164090: SARS-CoV-2 Semi-Quantitative Total Antibody, Spike using Roche Elecsys. <br /> Quest Test Code 39820 SARS-CoV-2 Total Antibody, spike, semi-quantitative using Roche Elecsys. <br /> With the huge # of publications on COVID-19, there should be articles correlating the level of IgG vs. breakthrough infections. Where is that article(s)??<br /> Stephen B. Strum, MD, FACP

On 2022-07-08 18:08:52, user Angel perez wrote:

This paper has been published in Applications and Applied Mathematics.<br /> The published version can be found at https://digitalcommons.pvam...

On 2020-11-17 01:51:32, user Chris Barker wrote:

Maybe I missed in the article. where is the formal definition of MAPE? and did you have access to the actual computer programs to run the projections or was it based on evaluation of the literature?

On 2022-01-12 20:54:58, user AGM wrote:

Yes, it does. The model does control for vaccination status along with many other covariates... it explicitly controls for vaccination status where possible (ie Omicron was so mild in some strata that there were not enough counts to do multivariate analysis). Per the manuscript:

"We repeated analyses of the symptomatic hospital admission endpoint within subgroups defined by patient age, sex, Charlson comorbidity index, and history of documented SARS-CoV-2 infection and vaccination, controlling for all other risk factors via covariate adjustment."

Also from manuscript:

"Reductions in disease severity associated with Omicron variant infections were evident among both vaccinated and unvaccinated patients, and among those with or without documented prior SARS-CoV-2 infection. Prior vaccination against COVID-19 was associated with a dose-dependent lower risk of detection of the Delta variant as compared to the Omicron variant; likewise, Delta variant infections were less commonly detected among cases with documented prior SARS-CoV-2 infection."

Read the article before commenting.

On 2021-02-06 10:16:20, user andreiakhmetzhanov wrote:

(SMs) I think the version of R is 4.0.3, not 4.3 :-)

On 2020-10-17 01:04:42, user Phyllis Magelky wrote:

This study says nothing about whether the groups were matched by ages/sex/ethnicity differences between the groups

On 2020-10-17 15:54:52, user Dan Myers wrote:

The results make sense, actually. Antivirals are usually not as useful unless used early.

On 2021-06-08 18:41:47, user Keith Flippen wrote:

Was there tracking of HIV viral load and T cell count during the infection and are numbers known prior to COVID?

On 2020-05-13 03:36:31, user Annalisse Mayer wrote:

But what about the people who died suddenly at home and never made it to the hospital? How many of them were smokers? Maybe being able to get to the hospital means one is better at resisting the infection

On 2020-03-30 13:57:15, user Sinai Immunol Review Project wrote:

Summary: Based on a retrospective study of 85 hospitalized COVID patients in a Beijing hospital, authors showed that patients with elevated ALT levels (n = 33) were characterized by significantly higher levels of lactic acid and CRP as well as lymphopenia and hypoalbuminemia compared to their counterparts with normal ALT levels. Proportion of severe and critical patients in the ALT elevation group was significantly higher than that of normal ALT group. Multivariate logistic regression performed on clinical factors related to ALT elevation showed that CRP >= 20mg/L and low lymphocyte count (<1.1*10^9 cells/L) were independently related to ALT elevation—a finding that led the authors to suggest cytokine storm as a major mechanism of liver damage.

Limitations: The article’s most attractive claim that liver damage seen in COVID patients is caused by cytokine storm (rather than direct infection of the liver) hinges solely on their multivariate regression analysis. Without further mechanistic studies a) demonstrating how high levels of inflammatory cytokines can induce liver damage and b) contrasting types of liver damage incurred by direct infection of the liver vs. system-wide elevation of inflammatory cytokines, their claim remains thin. It is also worth noting that six of their elevated ALT group (n=33) had a history of liver disease (i.e. HBV infection, alcoholic liver disease, fatty liver) which can confound their effort to pin down the cause of hepatic injury to COVID.

Significance of the finding: Limited. This article confirms a rich body of literature describing liver damage and lymphopenia in COVID patients.

Review by Chang Moon as part of a project by students, postdocs and faculty at the<br /> Immunology Institute of the Icahn school of medicine, Mount Sinai.

On 2020-12-07 13:02:33, user Fernando wrote:

Good morning, I have some comments: I couldn’t find the final D level at 7 and 10 days (hospital discharge), this information is crucial to establish the effectiveness of the ministered dose. <br /> At a first glance, considering the patients were mostly deficient in vitamin D and obese (slow D absorption) the dose provided seamed too low to produce results in such a short time (7-10 days), specially as it was vitamin D in its over the counter form (not calcifediol).<br /> Also not clear how many days after testing positive did the patients take vitamin D. It seems that in Brazil people are only hospitalized after aggravation.<br /> Thank You!

On 2020-11-27 21:02:26, user Robert Brown wrote:

Vitamin D, Magnesium, Steroids, PPI and COVID-19; Interactions and Outcomes - Response to ‘Effect of Vitamin D3 Supplementation vs Placebo on Hospital Length of Stay in Patients with Severe COVID-19: A Multicenter, Double-blind, Randomized Controlled Trial’ [Preprint] [1]

Thank you and congratulations on your important and significant paper. This is only the fourth[2] [3] [4] reported RCT examining vitamin D supplementation as a therapeutic intervention for COVID-19. Biology provides multiple pathways by which vitamin D hydroxylated-derivatives[5] may impact Covid-19 risks [including via; ACE2 receptors; airway-epithelial-cell tight-junction-function, immune responses [affecting lymphocytes, macrophages T cells, T helper cells, Th1, -17; Tregs; cytokine secretion IL-1, -2, -4, -5, -6 -10,-12; IFN-beta, TNF-alpha; defensins and cathelicidin, and receptors HLA-DR, CD4, CD8, CD14, CD38. Vitamin D also regulates; mitochondrial respiratory, inflammatory, oxidative and other functions; RXR and other receptor links between steroids, retinoids, hormonal vitamin D, thyroid hormone, oxidised lipids and peroxisomal pathway immune responses.][6]

Significant evidence [40+ patient-papers[7]] suggests higher Vitamin D status [serum/plasma 25(OH)D concentration] is associated with diminished COVID-19 infection rates,and reduced severity [including ICU admission and mortality].[2 3 4]

Thus, it is crucial, to consider if the preprint’s broad-based conclusion “Vitamin D3 supplementation does not confer therapeutic benefits among hospitalized patients with severe COVID-19”, [time to discharge as well as lack of observed ICU and mortality rate benefits], stands scrutiny when any one, or combination of, the following factors are considered: -

Delay in vitamin D administration after severe symptoms onset

Patients presented “10.2 days after symptoms”, thus were already verging on serious outcomes at admission; “89.6% required supplemental oxygen at baseline [183 oxygen therapy; 32 non-invasive ventilation] and 59.6% had computed tomography<br /> scan findings suggestive of COVID-19.” [Days to dyspnoea from overt infection average 7-8, and acute-respiratory-distress-syndrome [ARDS] develops after median 2.5 days.[8]]

Further, the timing of vitamin D supplementation, at or after <br /> hospitalisation, was not specified, despite timing clearly being an important factor, given the advanced stage of illness at admission.

Baseline vitamin D status [serum 25(OH)D concentrations] were relatively ‘good’

Baseline 25(OH)D values averaged 21.0ng/ml and 20.6ng/ml in the treatment and control groups respectively, i.e. they were relatively ‘good’, and above levels reported as being associated with the greatest COVID-19 risks.[9] [10]Sub-analysis of patients < 10ngml +/-Dexamethasone would be instructive. Further, deficiencies such as magnesium (an essential ‘D’ enzyme co-factor) might factor more in the lack of observed benefits for Covid-19 severity, than vitamin D status itself.

Corticosteroids

COVID-19 related corticosteroid vitamin ‘D’ interactions require<br /> investigation. 64.2%(Treatment) and 60.8%(Control) group patients respectively, were treated with Corticosteroids (Dexamethasone?), and mortality was somewhat higher in the Treatment than Control arm. Interactions between vitamin D and steroids including dexamethasone are observed[11], including “decreased synthesis of active vitamin D, and impairment of biological action at tissue level.”[12] However these potential effects have not been investigated in COVID-19 patients treated with both vitamin D and dexamethasone.

It would be most useful to know therefore, at what stage corticosteroid treatment began, and at what dosages, what other treatments were given [and at what dosage], and when such treatments were stopped, so that potential interactions between vitamin D, corticosteroids and other treatments for COVID-19<br /> patients could be elucidated.

In particular, any negative or neutralising effect of corticosteroids on<br /> ‘D’-derivatives and pathways, could account for the lack of reduction in risks of ICU and mortality outcomes, including slightly higher mortality, in those given vitamin D, a matter of importance, since dexamethasone, given before onset of serious ARDS, was reported in Oxford[13] to increase, not reduce, mortality.

Proton pump inhibitors.

PPI are known to lower serum magnesium,[14] an essential ‘D’ hydroxylase-enzyme co-factor. 47/120-(39%)[Treatment] and 49/120-40%[Control] used PPI, compared to 9.2% population usage in USA.[15] PPI-induced related serum magnesium reduction, +/- dietary insufficiency, is a reported COVID-19 risk factor,[16] thus possibly helping account, for D3 treatment, failing to reduce Brazilian Covid-19 mortality. Thought-provokingly a Brazilian paper reported “There is chronic latent magnesium deficiency in apparently healthy university students”, which deficiency is potentially more widespread.[17]

Conversely, RCT administration of magnesium with vitamin D reduced COVID-19 in-patient mortality.2

Rate of increase of Serum 25(OH)D

It is unclear when blood was sampled for determination of serum 25(OH)D concentrations, or if this was standardised for all patients.

A large bolus will increase 25(OH)D values in the healthy, “Oral D2 and D3 (100,000 to 600,000 IU) significantly increased serum 25(OH)D from baseline in all reviewed studies” . . . “peak levels were measured at 3 days (34) and 7 days following dosing,”[18]

However, timing matters, because hepatic hydroxylation5 to form 25(OH)D (Calcifediol) is likely reduced by; severe illness, as well as by obesity diabetes, and possibly hypertension,[19] conditions already recognised as risk factors for covid-19 severity.[20]

The Cordoba study[3] suggests that 25(OH)D [Calcifediol, that could be given together with vitamin D3, cholecalciferol], may be key to effective treatment of severe COVID-19 illness. There is no suggestion Cordoba patients were treated with corticosteroids. Cordoba patients were administered calcifediol on admission-day, but the period between overt infection and hospital admission <br /> was not reported.

Risk-factor Differentials in Patient Groups

A skew in risk factors favouring the control?

Control-Placebo to Treatment-D3:

Increased risk factors - Overweight (31/37, 0,84); Obesity (58/63, 0,92); Hypertension (58/68, 0,74); Diabetes II 35/49, 0,71); COPD (5/7,0,71); Asthma (7/8, 0,88); Chronic Kidney Disease (0/2, 0,0); Rheumatic Disease (10/13, 0,77)[21]; Black (14/20) Male 965/70).

Decreased factors - White (79/62) Female (55-50)

Improved oxygen parameters are not reflected in conclusion

“Despite the D3 group being at a greater risk, including due to hypertension, COPD and diabetes, known risk factors, significant differences in oxygen supplementation favour the D3 treatment group“.21

Oxygen supplementation (%) Placebo No. (%) D3 <br /> No oxygen therapy 9 (7.5) 16 (13.3)<br /> Oxygen therapy 97 (80.8) 86 (71.7)<br /> Non-invasive ventilation 14 (11.7) 18 (15.0)

Conclusion requires Caveats?

Thus, the un-caveated conclusion “Vitamin D3 supplementation does not confer therapeutic benefits among hospitalized patients with severe COVID-19”, likely requires caveats about possible effects of the several factors discussed above.

Further, the reported finding cannot be extrapolated to care of all Covid-19 patients, since the above- mentioned-potential interactions require further investigation, including; as to effects of; magnesium

status; treatment with PPI inhibitors, impact of corticosteroids in severe Covid-19 illness on vitamin D biology and outcomes, and consideration of pre-existing vitamin D status.

Further public health policy directed at reducing vitamin D, and other nutrient deficiencies for mitigation of COVID-19 risks at population levels, should not be conflated with clinical optimisation of vitamin D and metabolites for treatment of severe COVID-19 illness.

[1] Murai,I., Fernandes, A., Sales, L., Pinto, A., Goessler, K., et. al. 17th November 2020). Effect of Vitamin D3 Supplementation vs placebo on Hospital Length of Stay in Patients with Severe COVID-19 A Multicenter, Double-blind, Randomized Controlled Trial. medRxiv 2020.11.16.20232397; doi: https://doi.org/10.1101 /2020.11.16.20232397 Available at: https://www.medrxiv.org/content/10.1101/2020.11.16.20232397v1<br /> [2] Tan, C., Ho, L., Kalimuddin, S., Cherng, B., Teh, Y., et.al. (10th June 2020). A cohort study to evaluate the effect of combination Vitamin D, Magnesium and Vitamin B12 (DMB) on progression to severe outcome in older COVID-19 patients. doi: https://doi.org/10.1101/202... Available at: https://www.medrxiv.org/content/10.1101/2020.06.01.20112334v2<br /> Now published in Nutrition doi:10.1016/j.nut.2020.111017 <br /> [3] Entrenas Castillo, M., Entrenas Costa, L., Vaquero Barrios, J., Alcalá Díaz, J., López Miranda, J., Bouillon, R., & Quesada Gomez, J. (29th August 2020). Effect of calcifediol treatment and best available therapy versus best available therapy on intensive care unit admission and mortality among patients hospitalized for COVID-19: A pilot randomized clinical study. The Journal of steroid biochemistry and molecular biology, 203, 105751. https://doi.org/10.1016/j.j... Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7456194/<br /> [4] Rastogi, A., Bhansali, A., Khare, N., et. Al. (12th November 2020).<br /> Short term, high-dose vitamin D supplementation for COVID-19 disease: a randomised, placebo-controlled, study (SHADE study). Postgraduate Medical Journal Published Online First:. doi: 10.1136/postgradmedj-2020-139065 Available at: https://pmj.bmj.com/content/early/2020/11/12/postgradmedj-2020-139065<br /> [5] Bouillon, R., & Bikle, D. (2019). Vitamin D Metabolism Revised: Fall of Dogmas. J Bone Miner Res. 2019 Nov;34(11):1985-1992. doi:<br /> 10.1002/jbmr.3884. Epub 2019 Oct 29. PMID: 31589774. Available at: https://asbmr.onlinelibrary.wiley.com/doi/full/10.1002/jbmr.3884<br /> [6] Brown, R., Rhein, H., Alipio, M., Annweiler, C., Gnaiger, E., Holick M., Boucher, B., Duque, G., Feron, F., Kenny, R., Montero-Odasso, M., Minisola, M., Rhodes, J.,Haq., A, Bejerot, S., Reiss, L., Zgaga, L., Crawford, M., Fricker, R., Cobbold, P., Lahore, H., Humble, M., Sarkar, A., Karras, S., Iglesias-Gonzalez, J.,Gezen-Ak, D., Dursun E., Cooper, I., Grimes, D. & de Voil C. (April 20, 2020). COVID-19 ’ICU’ risk – 20-fold greater in the Vitamin D Deficient. BAME, African Americans, the Older, Institutionalised and Obese, are at greatest<br /> risk. Sun and ‘D’-supplementation – Game-changers? Research urgently required’: ‘Rapid response re: Is ethnicity linked to incidence or outcomes of COVID-19?’: BMJ, 369(m1548). DOI: 10.1136/bmj.m1548. Available at: https://www.bmj.com/content... (Accessed: 24 November2020. - Alipio study<br /> now in question – rest stands)<br /> [7] Brown R. (15 Oct 2020). Vitamin D Mitigates COVID-19, Say 40+ Patient Studies (listed below) – Yet BAME, Elderly, Care-homers, and Obese are still ‘D’ deficient, thus at greater COVID-19 risk - WHY? BMJ 2020;371:m3872 Available at https://www.bmj.com/content/371/bmj.m3872/rr-5 (Retrieved 24 Nov 2020) <br /> [8] Cohen, P., Blau, J., Eds: Elmore, J., Kunins, L., & Bloom, A. (2020). MD disease 2019 (COVID-19): Outpatient evaluation and management in adults. Literature review. Wolters Kluwner. Available at: https://www.uptodate.com/contents/coronavirus-disease-2019-covid-19-outpatient-evaluation-and-management-in-adults/print<br /> (retrieved 25th November 2020)<br /> [9] Jain, A., Chaurasia, R., Sengar, N., Singh, M., Mahor, S., & Narain, S. (19th Nov 2020). Analysis of vitamin D level among asymptomatic and critically ill COVID-19 patients and its correlation with inflammatory markers. Sci Rep. 2020 Nov 19;10(1):20191. doi: 10.1038/s41598-020-77093-z. PMID: 33214648; PMCID: PMC7677378. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7677378/<br /> [10] Radujkovic, A., Hippchen, T., Tiwari-Heckler, S., Dreher, S., Boxberger, M., & Merle, U. Vitamin D Deficiency and Outcome of COVID-19 Patients. Nutrients 2020, 12, 2757. Available at https://www.mdpi.com/2072-6643/12/9/2757 <br /> [11] Hidalgo, A. A., Trump, D. L., & Johnson, C. S. (2010). Glucocorticoid regulation of the vitamin D receptor. The Journal of steroid biochemistry and molecular biology, 121(1-2), 372–375. https://doi.org/10.1016/j.j... Available at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2907065/<br /> [12] Giustina, A., Bilezikian, J. (eds) (2018). Vitamin D and Glucocorticoid-Induced Osteoporosis. Vitamin D in Clinical Medicine. Front Horm Res. Basel, Karger, 2018, vol 50, pp 149-160 (DOI:10.1159/000486078) Available at https://www.karger.com/Article/Pdf/486078<br /> [13] The RECOVERY Collaborative Group. (17th July 2020). Dexamethasone in Hospitalized Patients with Covid-19 — Preliminary Report. J New England Journal of Medicine R10.1056/NEJMoa2021436 https://www.nejm.org/doi/fu... Available at https://www.nejm.org/doi/full/10.1056/NEJMoa2021436<br /> [13] FDA. (8th Apr 2017). FDA Drug Safety Communication: Low magnesium levels can be associated with long-term use of Proton Pump Inhibitor drugs (PPIs) https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-low-magnesium-levels-can-be-associated-long-term-use-proton-pump (Accessed 25th November 2020)<br /> [14] Hughes, J., Chiu, D., Kalra, P., & Green, D. (2018). Prevalence and outcomes of proton pump inhibitor associated hypomagnesemia in chronic kidney disease. PLoS ONE 13(5): e0197400. https://doi.org/10.1371/jou... Available at: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0197400<br /> [15] Lee, S., Ha, E., Yeniova, A., et. al. (30th July 2020). Severe clinical outcomes of COVID-19 associated with proton pump inhibitors: a nationwide cohort study with propensity score matching. Gut Published Online First: 30 July 2020. doi: <br /> 10.1136/gutjnl-2020-322248 Available at: <br /> https://gut.bmj.com/content/early/2020/07/30/gutjnl-2020-322248<br /> [17] Hermes Sales, C., Azevedo Nascimento, D., Queiroz Medeiros, A., Costa Lima, K., Campos Pedrosa, L., & Colli, C. (2014). There is chronic latent magnesium deficiency in apparently healthy university students. Nutr Hosp. 2014 Jul 1;30(1):200-4. doi: 10.3305/nh.2014.30.1.7510. PMID: 25137281. Available at: http://www.aulamedica.es/nh/pdf/7510.pdf<br /> [18] Kearns, M., Alvarez, J., & Tangpricha, V. (2014). Large, single-dose, oral vitamin D supplementation in adult populations: a systematic review. Endocrine practice: official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists, 20(4), 341–351. https://doi.org/10.4158/EP1... Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4128480/<br /> [19] Kheiri,B., Abdalla, A., Osman, M. et al. (2018) Vitamin D deficiency and risk of cardiovascular diseases: a narrative review. Clin Hypertens 24, 9 (2018). https://doi.org/10.1186 /s40885-018-0094-4 Available at https://clinicalhypertension.biomedcentral.com/articles/10.1186/s40885-018-0094-4 <br /> [20] Kruglikov, L,. Shah, M., Scherer, E. (Sept 2020). Obesity and diabetes as comorbidities for COVID-19: Underlying mechanisms and the role of viral-bacterial interactions. Elife. 2020 Sep 5;9:e61330. doi: 10.7554/eLife.61330. PMID: 32930095; PMCID: PMC7492082.<br /> [21] Borsche L. Private email 19.11.20

On 2020-07-13 09:32:26, user OxImmuno Literature Initiative wrote:

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

On 2025-08-22 02:16:48, user Dimitrios Kefalas wrote:

Thank you for this important piece of work and the opportunity to contribute with our comments.

To my understanding, factors that may affect the IONM diagnostic accuracy and/or comparability are the recordability of baseline(s), the monitorability of the signals, the repeatability and robustness, and how frequently the IONM signals are recorded.<br /> Maybe the above should also be reported.

Item 10a<br /> “…in sufficient detail for replication”<br /> Maybe it would help if this was more specific.<br /> What may not be clear to some IONM practitioners, is what is “sufficient” or not.<br /> I assume that all stimulation/recording parameters (and their changes during the procedure) should be reported, including the sequence of the modalities.<br /> For example, parameters that are not commonly reported and may affect diagnostic accuracy:<br /> Stimulation frequency, number of averages, and rejection threshold (for averaged signals).<br /> Application of special filters (e.g., smooth filter, on top of frequency filters).<br /> Increment of TES intensity following MEP drop.<br /> TES frequency, in case of trains of trains (some IONM practitioners may perform single-train TES, but is it still considered “single-train” if it is repeated manually?).<br /> Other factors that may affect MEP amplitude during the procedure, e.g., TES immediately after TES with different montage of immediately after SSEPs (while it was performed differently during baselines).

Item 22<br /> As it was mentioned on the introduction "...lack clarity regarding the timing of baseline data establishment".<br /> Similarly, the “time” (stage of the surgery) of the last IONM signal recording, of each modality, is not always reported. Undetected delayed ischaemia (because IONM was stopped early) would be considered a false negative. Reporting the time of the last IONM recording would improve the comparability of IONM studies.

On 2021-08-15 05:37:51, user disqus_Kj7WYajkfU wrote:

I'd like to know if there is other peer reviewed work on this on other <br /> similar situations. i am no expert but i don't think it takes a MD to <br /> figure out that making your 5 year old stay away from friends, family, school and other such activities and on top of all that wearing a face mask, which probably could cause issues with recognizing facial expressions etc...

On 2020-02-17 09:19:59, user Ellie_K wrote:

Keep this assessment of R0 values when making comparisons to other contagious disease, via the CDC in Atlanta https://wwwnc.cdc.gov/eid/a...

On 2021-09-03 13:39:22, user rbrine@msn.com wrote:

Since “each mRNA-1273 dose provides three times more mRNA copies of the Spike protein than BNT162b2”, why do recipients of mRNA-1273 require two doses for “full vaccination”, like recipients of BNT162b2, especially if the first mRNA-1273 dose caused a prolonged adverse reaction?

On 2021-03-15 17:04:19, user Eli Yazigi wrote:

Decoding Distinctive Features of Plasma Extracellular Vesicles in Amyotrophic Lateral Sclerosis

Key main ideas in the paper:<br /> • Nickel-Based Isolation (NBI) of extracellular vesicles (EVs) is an effective technique that both preserves the integrity of EVs and easy carry out in a clinical setting.<br /> • Extracellular vesicles in Amyotrophic Lateral Sclerosis (ALS) have distinctive features—in terms of size distribution and protein composition—that are different from EVs of patient with other muscular degenerative diseases (MD).<br /> • The amount of accumulated TDP-43 is indicative of the pace of progression of ALS. Increased accumulation of TDP-43 indicates faster progression of ALS in patients.

Main contribution to the field: The paper established that size distribution and composition of plasma extracellular vesicle can be reliably used to distinguish ALS from other muscular degenerative diseases.

On the scale of 5 (breakthrough) to 1 (no contribution to the field) I would rate the contribution of this paper at 4. The paper provides fast, reliable, and easy technique for isolation of EVs in clinical settings. Using this technique to analyze composition and size of EVs helps in making differential diagnosis.

The conclusions the authors draw in this paper follow experiments performed. And the assumptions made by authors are reasonable and well-thought. However, I think expanding the age range for participants to include younger patients would enhance the credibility of the data and provide for crucial insights.

One disadvantage of using NBI, is that it does not allow for isolation and distinction of extracellular vesicles that are generated through different biological processes (i.e., exosomes vs. microvesicles). These different types of vesicles are regulated in different manner and contain different cellular components.

On a scale of 5 (great) to 1(muddled), I would rate the writing in the paper at 4. There are few typos and grammatical errors. But for the most part the writing was clear and concise. I had to re-read the discussion section couple of times to understand to various conclusions and connect them together. Overall, algorithms are clearly explained in the paper. The logical follow in the paper is smooth and relatively easy to follow. Nonetheless, I think that the connection among various conclusions in the paper could better emphasized.

I think this paper will have a profound, lasting impact in clinical settings. It outlines the use a creative method to draw differential diagnosis among ALS and other MD diseases. The reliability and ease of method presented in the paper along with the data will prove to be revolutionary in the field of medicine.

On 2021-02-17 15:37:25, user Jules wrote:

Please review the pros and cons of using the names of birds (or any living animal) to differentiate between COVID variants. If a loved one dies from the bluebird variant, say, how might survivors feel when they see bluebirds? Might it not be a repetitive trigger for grief? And might not some people seek revenge on the birds? Furthermore, it is almostt inevitable that some will mistakenly think the birds carry or are responsible for COVID, putting robins and pelicans at risk the world over. And as Meredith rightly pointed out, it is damaging and most unfair to Robins everwhere.<br /> Why not use the names of colours? Or minerals? I am sure there are many alternatives that will serve the purpose.<br /> Having said all that, congratulations on your incredible work and contributions to public health. Thank you.

On 2020-09-29 10:51:15, user Sanal Madhusudana Girija wrote:

Beautiful and simple! <br /> 1) It is an interesting observation, that not only the cells in the lesion but also outside the lesion suffer from telomere shortening. This means even if the lesion is excised fresh lesions can appear near by. This is a significant observation. <br /> 2) In the malignant cells, may be if you have access to metastatic lesions, you should check for telomere length. I would not be surprised the telomere length would be again "normal" or even more than "normal" cells. <br /> 3) PBMCs were a choice for control. How about cells from another area if the IEC/IRC permits!

On 2025-04-16 09:01:39, user Idan Menashe wrote:

Now published here: https://doi.org/10.1002/aur.3085

On 2020-05-02 11:52:48, user Malcolm Lightbody wrote:

Hi, just wanted to say that this is an interesting piece of work. I think there is a typo in equation 1 - there should be a -ve sign in the exponent - as in c(t) = exp( - (t-T)^2 / tau^2).

On 2022-02-17 17:44:28, user BrianB wrote:

The Cosinor-based model used for season variation would be defined differently for those with deficiency versus sufficient concentrations. Also, after fitting the model to predict future concentrations, subjects may need to be reclassified into a different group (e.g., a sufficent subject with a sample taken in a bright period may be modeled as deficient in a dark period, and vice versa.) This was not indicated as being done, but should have been. Aside from that the Cosinor-based model is a rough model that has not shown to be consistent in predicting concentrations across populations. https://www.nature.com/arti...

On 2020-06-23 23:51:31, user Steve Moss wrote:

My initial concern after a very brief skim of the article, is that the raw data and statistical methods (including relevant code/parameters) aren’t available for reproducibility purposes. Could the preprint please be updated with links to these resources?

On 2020-06-25 11:12:33, user Dude Dujmovic wrote:

Faulty study. The BCG cohort is older than non-BCG cohort, likely by 2-3 years on average. That is not a small difference when the samples are so big. Amazing how they did not notice that. There is always a good reason why randomized samples are used. Your samples are biased based on age. You need to have samples with about the same average age and about the same standard deviation. And more.

On 2023-12-14 17:58:32, user Michelle Carras wrote:

Very curious about this. It's worth considering, but the authors had some big challenges with their sample, which is a relatively well-off, very White population, a bit older than the US average. They have a very high rate of premorbid asthma (about 2-4x the usual), but the thing I find most curious is the use of naltrexone (20% of the sample) and ivermectin (18% of the sample) to treat these new symptoms. Since these uses are very off-label, it makes me wonder about the types of patients who get them. Same with intermittent fasting as a non-pharmacological treatment. I'd be interested in seeing other responses to this and whether it ultimately gets published.

On 2021-08-23 17:44:20, user Olga Matveeva wrote:

Very interesting paper, however, I can't find supplementary material.

On 2020-08-16 19:15:38, user Skadu SkaduWee wrote:

One of the fundamental assumptions of the paper is the use of a previously tested positive saliva sample to prepare the serial dilutions used for the limit of detection studies. However, the authors omit to declare how this initial copies/ul value was arrived at and by whom.

On 2020-03-30 02:38:57, user Sinai Immunol Review Project wrote:

Summary of Findings: <br /> -Transcriptomic analysis using systems-level meta-analysis and network analysis of existing literature to determine ACE2 regulation in patients who have frequent COVID-19 comorbidities [eg- cardiovascular diseases, familial pulmonary hypertension, cancer]. <br /> - Enrichment analyses indicated pathways associated with inflammation, metabolism, macrophage autophagy, and ER stress. <br /> - ACE2 higher in adenocarcinoma compared to adjacent normal lung; ACE2 higher in COPD patients compared to normal. <br /> - Co-expression analysis identified genes important to viral entry such as RAB1A, ADAM10, HMGBs, and TLR3 to be associated with ACE2 in diseased lungs.<br /> - ACE2 expression could be potentially regulated by enzymes that modify histones, including HAT1, HDAC2, and KDM5B.

Limitations:<br /> - Not actual CoVID-19 patients with co-morbidities, so interpretations in this study need to be confirmed by analyzing upcoming transcriptomics from CoVID-19 patients having co-morbidity metadata. <br /> - As mentioned by authors, study does not look at diabetes and autoimmunity as risk factors in CoVID-19 patients due to lack of data; would be useful to extend such analyses to those datasets when available. <br /> - Co-expression analysis is perfunctory and needs validation-experiments especially in CoVID-19 lung samples to mean anything. <br /> - Epigenomic analyses are intriguing but incomplete, as existence of histone marks does not necessarily mean occupancy. Would be pertinent to check cell-line data (CCLE) or actual CoVID-19 patient samples to confirm ACE2 epigenetic control.

Importance/Relevance:<br /> - Study implies vulnerable populations have ACE2 upregulation that could promote CoVID-19 severity. Shows important data-mining strategy to find gene-networks associated with ACE2 upregulation in co-morbid patients. <br /> - Several of the genes co-upregulated with ACE2 in diseased lung might play an important role in CoVID-19 and can be preliminary targets for therapeutics.<br /> - If in silico findings hold true, epigenetic control of ACE2 expression could be a new target for CoVID-19 therapy with strategies such as KDM5 demethylases.

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

On 2021-09-24 00:58:51, user Blasto Labs wrote:

Dr. Gorski has been funded over the last decade by institutional funds, the Department of Defense, the National Cancer Institute, the Conquer Cancer Foundation of ASCO, and the Breast Cancer Research Foundation.

He has become the online spokesperson for the vaccine industry, a member of the highly trafficked, drug-industry-sponsored “Science”Blogs.

David Gorski has become the most outspoken, self-styled “skeptic” in defense of mercury that exceeds EPA limits in vaccine

On 2021-09-13 14:27:48, user Mike wrote:

There is a study titled "Risk of Myocarditis from COVID-19 Infection in People Under Age 20: A Population-Based Analysis" which has this conclusion:

"Myocarditis (or pericarditis or myopericarditis) from primary COVID19 infection occurred at a rate as high as 450 per million in young males. Young males infected with the virus are up 6 times more likely to develop myocarditis as those who have received the vaccine."

If we look at the overall COVID hospitalizations on CDC's COVID-NET, which covers 10% of the US population, it reports 3899 children (< 18) hospitalizations from COVID so far. Multipliying that by ten would take us to 38990 for the entire pandemic, so 18 months so far. So, on average, 8664 over 4 months.

There are 74.1 million children under 18 in the US, so that gives us a COVID hospitalization incidence of 116.9 per million for 4 months, on average, during the pandemic. If we extend that to 6 months, the average becomes 175.3 / million.

Even for the most affected demografic for the vaccine, 12-15 males, for which you calculated a risk of 162.2 per million after vaccination, the hospitalization risk would still not be higher than the average for children under 18, exposed to the average COVID risk for 6 months.

Unless the COVID hospitalization risk is much lower for the 12-15 age group compared to the entire < 18 age group, this seems to contradict the conclusions of your study.

Even if we assume boosters every 6 months, with the same type of vaccine, even for those that have already experienced this side effect after the first two doses (which could be easily avoided, just don't give boosters to those which experienced the myocarditis side effect), the benefits of the vaccine seem to be higher than the introduced risks, even for 12-15 males.

Looking at another metric, about 400 children under 18 died from COVID in the US, so far. I'm not aware of any dying after COVID vaccinations due to myocarditis, or other vaccine side effects.

On 2020-04-22 01:23:46, user michael triplett wrote:

Thank you again for your review, @Bio. I’ll follow your format in my reply.

1. I have no argument against the importance of the time variable when developing predictive models. However, this analysis was not intended to provide a stable predictive model of case rates as a function of time and temperature. It’s purpose was to provide a concise snapshot of case rates as they relate to a small set of high-level inputs. Excluding the time variable allows us to see the significance of other underlying factors. The analysis is also intended to provide that snapshot in a manner that can be thoroughly explained. And, I’m not sure which model has actually remained stable over time. Consider the continuous adjustments made to the famous IHME model, for instance.

To explain this another way, consider the kinematic equations for velocity. With the time variable included, v(t)=v(0)+a*t. As a function of position, v(s)^2=v(0)^2+2a*s. I’ve essentially presented this model as a function of position, rather than time.

1. You are correct that many other factors were omitted from analysis. It was stated in the introduction that no speculation was made outside of included data. The confounding factors you described are important, but including arbitrary adjustments can be equally confounding. “Expert opinion” is rarely better than “arbitrary” when applying quantitative correction factors. Binning of such a large sample size is generally more reliable than applying such correction factors to low-level data. Furthermore, to address the specific concern about lockdown measures, March 27 was inside the first two weeks for almost every country included. So, given the two week incubation period, lockdown measures could not have had a significant effect on case rates by that time.

2. I understand your point about low-level location, point-wise population mapping, etc., but I will just point to the binned data again. The sliding window approach has the effect spreading those point-wise populations and case rates so that such biases are minimized. It is not at all practical to map every case cluster, and adequate predictive data is unavailable at such a low-level. As for outliers, they were all in “cold” northern regions so omitting them actually made the analysis more conservative.

3. To address your point about temporal sequencing, which was my main concern with the data, it can be seen in Fig. 3 that case rates below -30 degrees also began to spike above tropical/equatorial regions. Travel patterns may have accelerated growth in that region, but the question then would be, “are travel patterns more/as significantly different by latitude than temperature?” And, given that the virus was in existence before humans began collecting data, it is likely safe to assume that travel-related factors are not terribly significant. Perhaps further study will tell. But, If this were a only a matter of origin and spread, the shared climates between northern and southern sub-tropical regions, as the seasons move through spring and fall, would also reduce significance of the temperature variable relative to latitude. I also struggle to imagine a real physical impedance to the virus’ movement through equatorial regions in the modern world. It originated in the northern hemisphere, but equatorial regions are skirted by large relative case rates on both sides. Maybe it isn’t effected by temperature directly, but it appears to be affected by a set of variables that are also correlated with temperature. That is really the point.

Finally, thank you again for your feedback. As stated in the conclusion, this analysis was intended to spur further research... not provide anything causal. Rather than rework what amounts to an out-of-date data set, I have taken your feedback and constructed a predictive model that accounts for the practically applicable variables you mentioned. I will be publishing the write up shortly.

In the meantime, we’ll see how things pan out.

On 2020-06-14 22:16:57, user Robert Clark wrote:

Truly puzzling. Experts in infectious disease know antivirals most effective when given early. Yet tests on antivirals that show effectiveness in vitro for COVID-19 continue to be tested on patients only under severe disease, where they are then found ineffective. <br /> This is a fundamental understanding for infectious disease experts in regards to antivirals for influenza and for HIV. Yet this is forgotten in regards to COVID-19.

Why?

Robert Clark

On 2020-10-17 11:52:14, user fvtomasch wrote:

I would add not only low sodium levels but low magnesium/zinc/potassium/B12/Vitamin D/and many essential nutrients depleted by medications people take for comorbidities of hypertension and diabetes like Metformin/HCTZ/PPI's which deplete these levels over time and basically opens Pandora's Box to having a more severe case of Covid and other diseases rather than having a mild or asymptomatic case if having proper or optimum nutrient levels. We are a over medicated society plain and simple. A pill for everything except good health.

On 2024-08-15 15:39:08, user Vanessa Merker wrote:

The final version of this article has been peer-reviewed and published online.

Citation: Chou C, Wiredu SO, Von Imhof L, et al. Health services interventions to improve the quality of care in rare disease: a scoping review. Therapeutic Advances in Rare Disease. 2024;5. doi:10.1177/26330040241262810

Available open-access at: https://journals.sagepub.com/doi/10.1177/26330040241262810

On 2020-07-27 03:48:45, user Hagai Perets wrote:

A potential explanation for such dynamics could be related to co-infectio, see <br /> https://arxiv.org/abs/2007....

On 2020-11-05 02:41:54, user Robert Stephens wrote:

This is a nice study!

"Interestingly, among children with symptoms compatible with COVID-19, only 11% (1/9) of those tested with RT-PCR were positive, while 60% (12/20) seroconverted. "

Perhaps some of the PCR -ve / seropositive children had gastrointestinal disease. Was there a pattern of symptoms for this group? Faecal / rectal PCR might have been interesting.

Dr Robert Stephens MB BS FACD

On 2021-06-03 12:25:21, user Johannes wrote:

"Lay persons are watching this study, and they say they love IVM and hate<br /> vaccine and let's use IVM instead of vaccine based on this study's <br /> result. <br /> "

Why ?

On 2025-10-17 18:54:43, user Jun Zhong wrote:

10/17/25 update: The article has been peered reviewed and it was published in Gut. Please cite this article as:<br /> Zhong J, O’Brien A, Patel MB, et al. Large-scale multiomic analysis identifies non-coding somatic driver mutations and nominates ZFP36L2 as a driver gene for pancreatic ductal adenocarcinoma. Gut, Published Online First: 08 October 2025. doi: 10.1136/gutjnl-2025-335152

On 2025-03-31 17:53:49, user Magalhaes Borges, Vini wrote:

The final version of this paper has been published on the JAHA webpage: https://www.ahajournals.org/doi/full/10.1161/JAHA.124.036193

On 2021-10-29 12:26:39, user Yehonatan Knoll wrote:

Good study of a bad question. <br /> Ten months into the vaxx campaign, why is there no similar, comprehensive study following vaxxed and unvaxed, *starting with the date of vaccination rather than that of infection*. This is the only pertinent question, now that a biannual booster is required of the vaxxed.

On 2023-04-21 15:29:37, user Erin Jonaitis wrote:

This manuscript has now been published in Brain Communications. The final version is available at https://academic.oup.com/braincomms/article/5/2/fcad057/7070362.

On 2019-11-10 21:15:52, user GuyguyKabundi Tshima wrote:

EVOLUTION OF THE EPIDEMIC IN THE PROVINCES OF NORTH KIVU AND ITURI AT 08 NOVEMBER 2019<br /> Saturday, November 09, 2019<br /> • Since the beginning of the epidemic, the cumulative number of cases is 3,286, of which 3,168 are confirmed and 118 are probable. In total, there were 2,192 deaths (2074 confirmed and 118 probable) and 1064 people healed.<br /> • 501 suspected cases under investigation;

THE LIST OF NO:

• No new cases have been confirmed;<br /> • No new confirmed deaths have been recorded;<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 161 (5% of all confirmed / probable cases), including 41 deaths;

NEWS

NOTHING TO REPORT

VACCINATION<br /> • Since vaccination began on August 8, 2018, 249,290 people have been vaccinated;<br /> • The only vaccine to be used in this outbreak is the rVSV-ZEBOV vaccine, manufactured by the pharmaceutical group Merck, following approval by the Ethics Committee in its decision of 20 May 2018.

MONITORING AT ENTRY POINTS<br /> • Since the beginning of the epidemic, the total number of travelers checked (temperature measurement ) at the sanitary control points is 115.036.328 ;<br /> • To date, a total of 111 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 2019-09-30 05:56:18, user Guyguy wrote:

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

The epidemiological situation of the Ebola Virus Disease dated September 27, 2019

Saturday, September 28, 2019

• Since the beginning of the epidemic, the cumulative number of cases is 3,186, of which 3,072 are confirmed and 114 are probable. In total, there were 2,128 deaths (2014 confirmed and 114 probable) and 989 people healed. <br /> • 446 suspected cases under investigation; <br /> • 3 new confirmed cases, including: <br /> • No cases in North Kivu; <br /> • 3 in Ituri, including 2 in Mandima and 1 Komanda; <br /> • No new confirmed deaths have been recorded; <br /> • No health worker is among the new confirmed cases. The cumulative number of confirmed / probable cases among health workers is 160 (5% of all confirmed / probable cases), including 41 deaths. • Vaccination rings were opened Friday, September 27, 2019 around confirmed cases of September 26 in the Mambasa Health Area located in the health zone of Mambasa in Ituri; <br /> • The satellite ring vaccination around the confirmed case of 20.09.2019 that started the disease in Beni continues in the health areas of Lisasa and Kalunguta in Kalunguta in the province of North Kivu; <br /> • Since the beginning of vaccination on August 8, 2018, 229,484 people have been vaccinated; <br /> • The only vaccine to be used in this outbreak is the rVSV-ZEBOV vaccine, manufactured by the pharmaceutical group Merck, following approval by the Ethics Committee in its decision of 20 May 2018. • Since the beginning of the epidemic, the total number of travelers checked (temperature measurement) at the sanitary control points is 99,958,288; <br /> • To date, a total of 111 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 2025-04-08 22:57:10, user Isada’s Biggest-Fan wrote:

It is very irresponsible that Cleveland Clinic ID made this available without peer review. There are multiple design flaws affecting the integrity of the study.

1. If the vaccine is mandated (all participants were CCF health workers) and we stop following patients who have been “terminated” it is very possible those who are “unvaccinated” and less likely to have the event because they were terminated/censored.

2. We are given little to no detail as to why some workers are getting vaccinated later than others (are those workers that get vaccinated more clinical and therefore have a higher exposure).

The discussion starts with “This study found a significantly higher risk of influenza among the vaccinated compared to the unvaccinated state in northern Ohio during the 2024-2025 influenza season.”

On 2020-05-26 06:03:55, user Hooman Noorchashm wrote:

Cyclosporine's generic status and global scalability as a potential effective therapeutic to block progression of COVID-19 disease is one of its most attractive attributes: https://medium.com/@noorcha...