On 2021-05-21 21:38:46, user lbaustin wrote:

Has this been submitted to a MEDLINE indexed journal?

On 2020-03-16 13:08:45, user Karl Milhon wrote:

I have been pushing for people to investigate the role of children in transmission very hard since the Chinese CDC first put out their descriptive epi piece. there are numerous articles and quotes pointing toward this element of Covid 19 transmission but it appears that no one is truly trying to get at the problem. Simply utilizing serology testing to do quick and dirty seroprevalence studies would provide some insight. Singapore has developed and utilized some decent serologic tests. I do not understand why this is not being more aggressively pursued.

On 2020-06-10 21:34:06, user DFreddy wrote:

Table 1 is missing? Also in additional material, an empty file

On 2020-11-23 11:57:37, user Martin Kral wrote:

Will this method effect any of the antibodies that the immune may have developed. In other words, after the infection has subsided, will the natural immune system develop the necessary antibodies or will a vaccine still be necessary?

On 2021-09-27 21:43:38, user Xem wrote:

Where does it say why it was withdrawn?

On 2022-01-02 23:31:07, user Florian Binder wrote:

Very interesting hypotheses and analyses.<br /> Did you also check for an effect of absolute humidity?<br /> As the air is quickly warned up when breathed in, this might influence the amount of virus material breathed out.

On 2020-03-20 00:15:32, user RKM wrote:

The second paragraph in bold blue in this article says it all, "yet to be evaluated."

Is it 2 days, 9 days, do you really know?

The CDC is telling us this:<br /> https://www.cdc.gov/coronav...

But research tells us something completely different:<br /> https://www.news-medical.ne...<br /> If you have problems with the following link, then click on the link above and scroll down to the link that says, “The Journal of Hospital Infection.” <br /> https://www.journalofhospit...

On 2021-07-23 12:04:42, user Harry Matthews wrote:

Very fascinating work. I read it with great interest. I think some Supplementary Tables are missing, though. In the supplementary pdf I see up to Supplementary Table 3. But in the caption of main figure 5 there is reference to a Supplementary Table 6.

On 2020-05-17 22:30:47, user Arvind Gulati wrote:

There is a new randomised controlled double blinded trial of 2000 participants starting sponsored by NED unfortunately they are not adding ZINC which seems to make the key difference. I don't know how to connect the study sponsors.

On 2021-08-24 08:23:27, user Meerwind7 wrote:

I like to praise that an assessment like this is possible only in a "No-Covid" environment where extensive contact tracing of individual cases is possible.

The conclusion about the difficulties to contain transmission even in this setting, i.e. with rare infections that allow extensive contact tracing ("individual-based interventions such as case isolation, contact tracing and quarantine"), points to the near-impossibility to contain Delta in the larger part of the world, even with more voccination.

On 2025-02-05 17:22:07, user Daniela Oliveira wrote:

Published: https://doi.org/10.1093/brain/awae088

On 2025-02-21 05:14:49, user Evan Stanbury wrote:

A Machine-Learning (ML) model was able to distinguish fairly well between the "sick" and "not sick" cohort. But most ML models are incapable of explaining why a decision was made.<br /> In particular, ML cannot distinguish between the following two hypotheses: (A) "PVS is a Post-Vaccination Syndrome" (ie Iatrogenic) vs (B) "PVS is a Post-Viral Syndrome" (ie a symptom of disease). This is an important distinction since the the reported training data does not include patients with Long COVID.

On 2025-03-01 16:56:25, user andreaclovephd wrote:

Does this actually identify persistent immune dysfunction after COVID-19 vaccination? No.

The big takeaways:

The study did not accurately correct for past infection. The methods used to “exclude” past infection is not accurate–the data presented suggest everyone has similar history of past infection, which means the PVS symptoms reported by participants cannot be attributed to vaccination.

The study didn’t actually assess T cell exhaustion. This would have needed to show markers of T cell exhaustion (TIM-3, CTLA-4, PD-1, etc) combined with impaired function: cytokine levels, <br /> proliferation, metabolic defect, & gene expression changes. They don’t do any of this. IFN-? and TNF-? are comparable between groups and suggest activated T cells, not exhausted.

They did not use a method to assess EBV reactivation. They assess serology, not EBV replication, which is required to show reactivation.

CD4 T cell populations aren’t meaningfully different between groups & are within normal ranges for healthy individuals.

On 2021-08-29 08:15:47, user Jeroen Boschma wrote:

The group of unvaccinated persons are truly survivors of their first infection, this means that many of the weak and problematic health cases have died during their first infection and are no longer present in that group. If Covid has a mortality of 1.5%, then this subgroup is 240 cases for the 16000 large group. However: all those cases of weak and problematic health who likely die from an unprotected infection are still present in the group of SARS-CoV-2-naïve vaccinees. So a selection was done where the most vulnerable persons were taken out of the unvaccinated group (death), but that selection is not done in the vaccinated group simply because it is not possible to predict at forehand who will die from an unprotected Covid infection. Although the groups are finally selected on equal risk factors, the above observation will always introduce a huge statistical bias.

I am quite sure that the group of cases found in the 'vaccine' group are largely those persons who would have died from an unprotected Covid infection. Because those persons are by definition not present in the unvaccinated group (they died during the first infection) you can explain the number of cases in both groups precisely by the above described mechanism. The conclusion then is that the found cases have nothing to do with 'better resistance due to an earlier infection'.

EDIT: I see now below that William Richard Dubourg made the same comment about the deaths due to Covid. I had problems with my Disqus account and could not post for a couple of days. Moreover: yesterday I saw 0 comments below this article while today suddenly comments appear that are 3 days old. Strange behavior....

On 2021-08-30 20:34:53, user Jason Anderson wrote:

I am from the opinion that this type of article being available before being peer-reviewed is slightly irresponsible due to the amount of news coverage it is likely to receive. After reading the manuscript, if I were reviewing, it would be a strong reject or major revisions (depending on the opinion of the handling editor). My expertise is certainly not medicine, but it is on data science and advanced statistical/econometric methods - the precise methodology the authors used here. To keep it short, splitting the data and generating separate models is not appropriate in this context based on the discrete outcomes the authors are modeling. IF, and big if, the authors are going to defend having separate models, there are a series of tests that need to be done to show that this is the appropriate approach. This is lacking. Also quickly, the authors have done their best at controlling for what they can, but there are still numerous unobservables that are not accounted for. Why is this important - it can bias parameter estimates, which leads to ORs (calculated from parameter estimates) that are not true representations of the population parameters. ORs can also be misleading; hence, the preferred inference is based on marginal effects.

If anybody, including the authors, are interesting in additional, more detailed comments, I'd be happy to discuss.

On 2021-10-30 04:38:45, user Rn wrote:

The conclusions of this study stand in stark contrast to a report published today by the US CDC. https://www.cdc.gov/mmwr/vo...

Among COVID-19–like illness hospitalizations among adults aged >=18 years whose previous infection or vaccination occurred 90–179 days earlier, the adjusted odds of laboratory-confirmed COVID-19 among unvaccinated adults with previous SARS-CoV-2 infection were 5.49-fold higher than the odds among fully vaccinated recipients of an mRNA COVID-19 vaccine who had no previous documented infection (95% confidence interval = 2.75–10.99).

On 2022-02-12 20:26:12, user Jan Lakota wrote:

This paper is in concert with the presented findings:<br /> New diagnosis of multiple sclerosis in the setting of mRNA COVID-19 vaccine exposure

J Neuroimmunol. 2022 Jan 15;362:577785. doi: 10.1016/j.jneuroim.2021.577785.

On 2020-09-18 16:27:11, user kdrl nakle wrote:

These types of papers that are masquerading as science are nothing more than speculations. Even IMHE forecasts from this Spring are laughable now. This is in the same venue.

On 2021-07-05 20:17:46, user Baljeet Singh wrote:

The trial data looks good and with sufficient details for analysis.

On 2023-01-23 00:20:10, user Stephen Akar wrote:

I think this is a fantastic work by this great team. I am working on YF in Nigeria.

On 2020-05-01 20:49:37, user Sinai Immunol Review Project wrote:

Title: The phenotypic changes of ?? T cells in COVID-19 patients

Keywords

Innate immune response, CD25, ?? T cells.

Main findings

?? T cells represent 1-10% of total circulating lymphocytes, and are able to promptly respond to infections and other stimuli. To address the effects of SARS-CoV-2 infection on ?? T cells, the authors collected blood samples from 18 healthy donor (HD) s and 38 COVID-19 patients and analyzed the frequency and phenotype of ?? T cells.

Unlike other viral infections, COVID-19 patients presented lower frequency of circulating ?? T cells than HD. Among ?? T cells, there was an increase in the CD4+ subset and CD25 expression compared to non-infected volunteers. The authors also report that ?? T cells of COVID-19 patients didn’t present higher frequencies of early activation/exhaustion markers such as CD69 and PD-1, in comparison to the control group.

Limitations

There is very little information on COVID-19 patients or healthy volunteers (age and sex should be reported). Furthermore, since the time after the onset of symptoms and viral load may be important parameters in the innate immune response to SARS-CoV-2 the authors should have shown this information in a table.<br /> Since lymphopenia is an important characteristic of COVID-19 patients [1] and the authors observed lower frequencies of ?? T cells, it would have been important to show frequencies and cell numbers for different T cell populations.

Relevance

This study indicates, for the first time, that ?? CD4+ CD25+ T cells can be involved in the acute phase of COVID-19. The function of ?? T cells in the context of COVID-19 should be further investigated.

References

1. Tan, L., et al., Lymphopenia predicts disease severity of COVID-19: a descriptive and predictive study. Signal Transduct Target Ther, 2020. 5(1): p. 33.

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 2021-10-03 07:08:57, user kdrl nakle wrote:

Midwestern state? Write South Dakota, what is the point of obfuscation? A lot of stuff in this paper, nothing usable.

On 2021-12-29 01:23:50, user lowell2 wrote:

The negative estimates in the final period arguably suggest different behaviour and/or exposure patterns in the vaccinated and unvaccinated cohorts causing underestimation of the VE. --uh, evidence that suddenly at 91 days people started behaving differently than they did the previous 90 days? this conclusion in the discussion has no substantiation whatsoever. Maybe the vaccine just didn't work after that regardless of what people did or didn't do.

On 2020-02-15 21:55:51, user Nate wrote:

It does need to be pointed out that this is Pre-Print at this point in time. It still needs to go through peer-review, etc., to be published.

That said, if this research is borne out/validated then this is pretty problematic news. The Chinese Government gave an R0 value of 2.6-2.9 or something like that, and also has publicly said the mortality rate is similar to the 2006 SARS outbreak (which had a lower R0 of something like 1.9 or something (possibly lower) ultimately. Assuming these figures are more accurate, If the Chinese Government is either not finding or hiding the number of cases but not the number of deaths, it actually may be good news, as the mortality rate would be considerably lower. However if they are wrong about or lying about both figures and it is both more contagious and more deadly, this could be a pretty serious epidemic/pandemic. If they, for instance are underestimating or underreporting the mortality rate by about .5 deaths per 1000 (I believe that’s the metric I’ve seen), the mortality rate would be roughly that of the 1918 Spanish Flu. Now, we are far better at treating symptoms now and preventing person to person spread of disease as we were in 1918, as well as developing vaccines. We have a lot of developed treatments that could be effective in minimizing symptoms or fighting the disease as well, even short of a currently viable cure/particularly effective treatment.<br /> However, that R0 value, if anywhere close to on target is pretty alarming. Even if the actual value is halfway between China’s figures and this study’s figures, and even if it were merely as deadly as SARS was.

Still, this isn’t an official figure yet. This isn’t even published, we don’t know how much other research will validate this number or contest it. So don’t panic based on a pre-print article. This probably has more value being available for other researchers, whom seeing other people’s figures, or methodology could benefit in their own research or methodology, and public heath officials who need to try to assess what a worst case scenario may look like. If these figures are accurate, they would be alarming. Even somebody who can read statistics and the language correctly in shouldn’t simply take something like this as fact, until it gets through peer review, other experts evaluate it once it’s published, and other figures start to align with their findings. I engaged in speculation, as it is really concerning should these figures be correct, and an interesting conversation to engage in. However, I am not credentialed in epidemiology, public health, or medicine. You should listen to experts and public health officials, over then speculation of somebody like myself. I am discussing the implications of this if true, not rendering an expert opinion.

On 2021-08-11 20:20:37, user amalio telenti wrote:

Please check the text: purifying selection = negative selection

On 2022-10-26 14:42:42, user Barbara Arch wrote:

Following peer review, the results and conclusions presented in this paper are currently under review. Further analysis is being undertaken and we will update the paper on completion of this additional work. <br /> Barbara Arch (lead author) & Prof MG Semple (Senior author and Study Sponsor CI)

On 2022-01-05 16:39:51, user Mike B wrote:

This is obsoleted by the Omicron variant.<br /> Publication of this data may be misleading due to the immune escape of Omicron being much higher than Delta.

On 2020-08-08 14:40:16, user Jomar Fajardo Rabajante wrote:

This is already published in Dy, L.F., Rabajante, J.F. A COVID-19 infection risk model for frontline health care workers. Network Modeling Analysis in Health Informatics and Bioinformatics 9, 57 (2020). https://link.springer.com/a...

On 2020-04-07 13:31:01, user Jaco Brand wrote:

I see clinical trials being initiated based on a paper that have not been peer-reviewed or published. The trend with income can be interpreted in a myriad of different ways, like lifestyle choices and diet. This is exactly why Fig. 3 show a different death rate between low and medium-high income countries, despite both groups having a universal BCG vaccination policy. This is a highly unscientific speculative statistical correlation study. I have highlighted further comments to the paper as a download

On 2020-03-31 15:52:10, user Pedro Thompson wrote:

Is it valid to compare an Italy with a destroyed health system against a Brazil just beginning the problem? I mean, is the mortality rate a constant, in the same country during all the epidemic?

On 2020-04-12 00:48:21, user Oleg Gasul wrote:

I am not sure about data correctness from the countries Turkmenistan, Uzbekistan and Kazakhstan, but all of them have very small number of cases (event zero in Turkmenistan).

But if we take a look on the map http://www.bcgatlas.org/ there is information that all of them have "Multiple BCG". That I understood the BCG vaccination is carried out several times (After birth, 6-7 yrs and 15 yrs).

On 2021-03-26 17:47:12, user ayman alqunneh wrote:

• This article represents one of the most robust, well-organized studies I have ever read and reviewed.
• Its large sample size gives the article a high level of reliability and trust.
• Although the results of this study did not significantly differ from other studies published in this field, its focuses on Arabic-speaking communities gives its uniqueness and makes it special.
• Elements assessed by the researcher and his colleagues were inclusive and well selected.
• Inclusion and exclusion criteria for individuals selected to be included in the analysis make research unbiased.

On 2021-03-11 20:59:15, user External Reviewer wrote:

The authors recruited their survey participants through a digital campaign on social media. However, the paper does not mention the specific social media platforms or accounts which were used to promote the survey and the potential impact of these accounts on the validity of the study.

The survey was mainly advertised on the first author’s Facebook page which has close to 2.8 million followers and on his YouTube channel which has close to 875,000 subscribers. This explains the massive sample size and the clear bias in the results. In particular, the first author is a well-known science-denier who has been pushing a pseudoscientific creationist perspective onto his social media followers for years.

There is absolutely no surprise that the results came out the way they did. The majority of the survey participants were skeptic of the vaccines and had a general distrusting view of pharmaceutical companies. These people have been conditioned (socially influenced) for years by the first author to believe that the “atheist west” was conspiring against them. At this point, it is almost impossible to convince them otherwise.

Finally, a message to the reviewers, unless the authors provide an evidence to debunk my claims, please do the right thing. This paper should be rejected.

On 2021-11-02 11:31:33, user Tom Jefferson wrote:

The review has now been published in Clinical Microbiology and Infection: https://doi.org/10.1016/j.c...

On 2020-04-23 05:57:15, user David Feist wrote:

It is always good to compare data within nations. But in fact preliminary, linear regression analysis, from a fellow maths major, now seems to indicate that the lockdowns had no statistically significant effect within the USA: https://www.spiked-online.c....

This Santa Clara study indicates why Sweden, Japan, South Korea and Australia have not had public health apocalypses, with no lockdowns; the mortality rate was miscalculated.

On 2020-04-23 04:46:38, user Dennis Maeder wrote:

Although flawed, this emphasizes the need for good representative sampling and antibody testing and the strong possibility that current case counts are wildly underestimated.

On 2020-04-22 01:33:09, user peteolcott wrote:

People on the internet are using this study to actively promote very risky behavior. Here is my analysis that rebuts this study:

Conclusive proof that covid-19 is much more lethal than the flu is provided by the fact we already have more deaths than the seasonal flu even though we took unprecedented precautions to minimize these deaths.

37,889 2020-04-18 USA covid-19 deaths<br /> 34,200 2018–2019 influenza season deaths

If we reduce the number of human interactions 50-fold and still have more deaths than the seasonal flu this conclusively proves that covid-19 is 50-fold more deadly than the seasonal flu.

This is true no matter what the per infection death rate is. If the per infection death rate of covid-19 is the same as the flu yet the unmitigated infection rate is 25-fold greater than the flu, then covid-19 is still 25-fold more deadly than the flu.

On 2020-04-19 03:40:52, user disqus_B1vk25qxNZ wrote:

Possibly other coronaviruses that the population has been exposed to confer cross immunity to SARS-CoV-2. If so, the benign virus could be a vaccine analogous to cowpox and smallpox.

On 2020-04-28 09:36:54, user DaveSezThings wrote:

The error the authors have made is a basic one in the propagation of uncertainty. We have a test kit which has some uncertainty regarding its performance, hence the confidence intervals on the specificity and sensitivity of the test. These confidence intervals are established by the manufacturer's trial using 85 confirmed positive and 371 confirmed negative samples and the author's tests on 37 RT-PCR-positive samples and 30 pre-COVID samples. Without further testing of the test kit using known samples there is nothing that can be done to change the confidence intervals for the sensitivity and specificity - it doesn't matter how many samples are tested for the main study. However, this is not correctly represented in the author's calculation of the propagation of the uncertainty by the author's. In their work they use the variances for the individual binomial distributions, compute the combined variance on this basis (called Var(pi) in the appendix) and then to get the standard error by taking the square-root of this combined variance divided by themain study sample size 3,330: SE(pi)=sqrt(Var(pi)/3330)=0.0034. This is incorrect. It confuses the variance of binomial distributions with the uncertainty regarding the estimate of parameters which will be binomially distributed. The author's should have been computing the square of the standard error using the delta method and replace each of the terms Var(q), Var(r) and Var(s) with their respective standard errors-squared (which will bring in some different n's for the various studies, although it'll be a bit more complicated for Var(r) and Var(s) given that more than one study has been combined to get these). This will give a much larger standard error for pi - the test-kit corrected prevalence. Alternative/better methods than the delta-method will yield the same result and it's such a large change that it essentially reduces the study to an upper-limit estimate only... the lower limit goes down to zero (or very close to zero).

It seems there are many other concerns as well regarding the sampling <br /> method and technical details of the serology but I'm not able to comment<br /> on those. I'm actually an optical physicist so I just have an amateur interest in this but a basic mathematical error is a basic mathematical error and that's what they've done. It's that bad. Looking through the comments here the point has been made many times in one form or another. There are 17 authors on this - it should take less than a day for one of them to correct the results and re-write the conclusions. It's no longer an interesting outcome of course - but it's scientifically the right thing to do - the fact that things are hurried because of the pandemic excuses errors but not quick correction once these have been pointed out. And there is no debate on this one - I might not be articulating the argument as well as others can and of course there are better analysis techniques than the delta method - but as sure as 2+2 isn't 5 their standard error for these results isn't what the authors claim. It's a big whoops - I hope the author's go easy on whoever of them made the mistake as I can well understand the time pressures surrounding this work. The classy thing to do is for all of them to take collective responsibility, issue the correction and move on from there.

On 2019-11-14 14:53:08, user Guyguy wrote:

EVOLUTION OF THE EPIDEMIC IN THE PROVINCES OF NORTH KIVU AND ITURI ON NOVEMBER 12, 2019

Wednesday, November 13, 2019

• Since the beginning of the epidemic, the cumulative number of cases is 3,291, of which 3,173 are confirmed and 118 are probable. In total, there were 2,193 deaths (2075 confirmed and 118 probable) and 1067 people cured.<br /> • 508 suspected cases under investigation;<br /> • 4 new confirmed cases in North Kivu, including 2 in Beni and 2 in Mabalako;<br /> • No new deaths of confirmed cases have been recorded;<br /> • No cured person has emerged from ETCs;<br /> • No health worker is among the new confirmed cases. The cumulative number of confirmed / probable cases among health workers is 163 (5% of all confirmed / probable cases), including 41 deaths;

NEWS

Ebola Virus Disease Response Coordinator Meeting with North Kivu National Assembly Vice President on J & J Vaccine

• The General Coordinator for the Ebola Response to the Ebola Virus Disease, Prof. Steve Ahuka Mundeke, accompanied by a joint team of some members of the response and the consortium (National Institute of Biomedical Research-INRB, MSF / France and the London School), met this Wednesday, November 13, 2019 the Vice President of the North Kivu Provincial Assembly, the Honorable Jean-Paul Lumbulumbu, with whom they discussed the second Ebola vaccine called Johnson & Johnson.

• The Professor Steve Ahuka Mundeke, who requested the involvement of elected representatives in the community mobilization for this vaccination, welcomed the availability of the Provincial Assembly of North Kivu to support the activities that will begin on Thursday, November 14, 2019 in two health areas of Karisimbi, namely Kahembe and Majengo in North Kivu Province;

• In addition, the Honorable Jean-Paul Lumbulumbu promised to be among the first people to be vaccinated with the Johnson & Johnson vaccine, including members of the North Kivu Provincial Assembly, to serve as an example for their bases. To this end, he invited the people of North Kivu, particularly the sites concerned, to be vaccinated in order to protect themselves against any possible epidemic of the Ebola Virus Disease;

• Also in the context of the introduction of this second vaccine, a briefing session was organized on the same Wednesday in the meeting room of the general coordination of the response in Goma, for members of the Risk Communication. and community engagement (CREC) with some partners from the Ministry of Health.<br /> Training of Beni journalists on their role and responsibility in public health emergencies.

• The role and responsibilities of the journalist in the treatment of news in a public health crisis is at the center of this workshop held from 12 to 14 November 2019 in Beni, North Kivu Province;

• This workshop aims to equip about twenty media professionals with essential notions related to the treatment of information during a health crisis;

• At the opening of this meeting, the feather knights were trained on the risk communication related to Ebola virus disease and on the usual concepts in the response to this disease;

• The two speakers of the day, Dr. Bibiche Matadi, who is responsible for the surveillance pillar at the sub-coordination of the Beni response and Mr. Rodrigue BARRY of the WHO, emphasized the quality of the message to be given to because, according to them, the eradication of this epidemic is based on mastery of all contacts and on community involvement;

• The second day focused on journalist ethics and deontology in times of health crisis and on health - communication - media interaction;

• For this second topic, Ms. Miphy Buata, a journalist with the Congolese News Agency and communications officer of the Multisectoral Committee for the Response to the Ebola Virus Epidemic, recalled that the media remains the only channel of choice to restore and build trust between the (recipient) community and the health sector (Issuer), particularly in the context of Ebola Virus Disease;

• This workshop was organized by the Ministry of Health with WHO and was facilitated by UNICEF.

VACCINATION

• Since the start of vaccination on August 8, 2018, 251,079 people have been vaccinated;

• The only vaccine to be used in this outbreak was 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

• Since the beginning of the epidemic, the total number of travelers checked (temperature measurement ) at the sanitary control points is 116,596,285 ;

• To date, a total of 112 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 2019-11-09 20:30:28, user GuyguyKabundi Tshima wrote:

EVOLUTION OF THE EPIDEMIC IN THE PROVINCES OF NORTH KIVU AND ITURI AT 07 NOVEMBER 2019<br /> Friday, November 08, 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 /> • 560 suspected cases under investigation;<br /> • No new confirmed cases;<br /> • No new confirmed deaths have been recorded;<br /> • 1 person cured out of the CTE of Butembo;<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

End of tour of the general coordinator of the Ebola response in North Kivu and Ituri

• The Epidemic Response Coordinator for Ebola Virus Disease, Prof. Steve Ahuka Mundeke, was on mission from 05 to 07 November 2019 in a few areas affected by Ebola Virus Disease in North Kivu and Ituri, to inquire about the epidemiological and security evolution of the response. During this mission, he visited some sites of the response to Beni in North Kivu, including the Mangango camp where the vaccination of pygmies took place;

• In Ituri, Prof Ahuka traveled to Biakato Mines in Mandima, Mambasa Territory, where he first reinserted three of the four cured patients he had discharged well into the Mangina Ebola Treatment Center in the area. Mabalako health center in North Kivu. He also comforted the family of the retaliating agent and journalist, murdered on the night of Saturday, November 2, 2019 in Lwemba in Mambasa territory in Ituri;

• He also chaired the daily meeting on the activities of the response in the sub-coordination of Biakato Mines;

• On his way back, the general coordinator of the riposte went to the Mangina Subcommittee, where he chaired under the trees the morning meeting in Mangina. He also visited the Health Center "Case of Salvation" which collaborates with the response and to whom he handed over a large batch of mattresses in the presence of the WHO coordinator of Mangina's sub-coordination. He again visited the Mangango camp, where the pygmies who have joined the activities of the riposte live to help the response reach all the other pygmies;

• He closed his tour of North Kivu and Ituri with a visit to the Ebola Treatment Center in Beni.

VACCINATION

• Pygmy vaccination continues in Mabalako at Mangango camp, 19/19 vaccinated pygmies;<br /> • Continuation of vaccination in expanded ring, around 3 confirmed cases on 04/11/2019 and 2 cases confirmed on 05/11/2019 and the vaccination of the biker as contacts, in Beni in five (5) areas health care, including in Butsili, Ngongolio, Tamende, mandrandele and Kasabinyole;<br /> • Since vaccination began on August 8, 2018, 248,460 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

• Since the beginning of the epidemic, the total number of travelers checked (temperature rise) at the sanitary control points is 114,626,335 ;<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 2025-03-14 14:22:15, user Amir wrote:

The paper’s statistical approach is troublingly opaque; without a detailed account of the one-way ANOVA assumptions or the Prophet model’s parameter choices, the reported findings on vaccine delays and excess mortality remain unconvincing and methodologically fragile.

While the manuscript highlights a correlation between delayed vaccination and excess deaths, it fails to adequately control for crucial confounding variables such as healthcare infrastructure, socioeconomic status, and demographic differences, making its causal claims appear overly simplistic.

Claiming that 50,000 excess deaths resulted directly from delayed vaccination campaigns is a bold assertion that lacks the necessary evidentiary support; the absence of comprehensive sensitivity analyses and diagnostic metrics renders this figure speculative at best.

On 2020-04-16 00:27:24, user Adam Danischewski wrote:

China has a BCG Vaccination policy and there may be other aspects that may cause Chinese results to differ from the United States.

On 2021-03-16 00:48:29, user Brian wrote:

The main conclusion is driven by a particular 14 day past 2nd dose counterfactual which does not seem realistic in the context of other data. These are the are the graphs in the supplementary material. It makes VE look higher than it likely is during that timeframe. Otherwise results inline with other papers.

On 2020-06-21 12:07:15, user Isaac Nault wrote:

I'd be interested to see this methodology applied to estimating hospitalization rate.

On 2025-04-09 12:24:29, user Breck wrote:

My colleague wants to know why you didn’t mention any testing for the flu. Did you test for the flu?

On 2020-05-08 15:43:56, user Ryan Pavlik wrote:

This looks like a lot of work and some valuable data. The main question that came to mind when reading it was "What defined a 'pre-COVID' control?" There's one reference in the in-house ELISA procedure (in this version, in supplementary material) that a control was a "pre-July 2018 historical Negative Control serum from two donors", but there's no description in the main paper on this point. The reference cited when describing the controls was your earlier paper on Chagas disease testing, which I took to imply that the same control samples were used, but I think this might be better made explicit. Given what we're finding about earlier world-wide spread, it would be valuable to state the date that's being considered pre-COVID to avoid doubt.

(It's fascinating, although on reflection unsurprising, that the antibody tests appeared to have found some false-negatives according to PCR testing. I appreciated that result being highlighted.)

Thanks for all the work you're doing!

(PS: different-field academic here, immunology is definitely not my thing, so if this comment isn't applicable for some field-specific reason, I apologize for the distraction.)

On 2020-04-22 03:21:20, user JC wrote:

Can you provide any details about how much of the drug you gave each patient? It’s quite odd that it wasn’t included in this study. Especially, since it’s already known in high doses it can cause problems for patients, and if too low it wouldn’t make a difference.

On 2020-04-21 19:40:16, user Brandon B wrote:

Risk of ventilation was 6.9% in HQ + AZ group and 14.1% in no Tx group. That is double. It was stated that these numbers are similar in the article. Not significant?

On 2020-04-21 23:42:55, user deutsch wrote:

The group no HCQ had azihtromycine 31% !!!!

On 2021-01-23 20:40:07, user 1ProudPatriot wrote:

Thank you so much for engaging in this work. Desegregated data is so difficult to find in many sub-populations. It would be interesting (although there is likely limited or no funding resources for this) to see this data in a table alongside of other respiratory illnesses. My other wonder is in the evaluation of whether or not to have my daughter participate in the vaccine at this point. We have typically had her take the flu shot, but given the elevated adverse responses the vaccines have had when compared to the flu, it would be helpful to have a resource by which we can evaluate our decision. Thank you again. I just found out about his website and am grateful!

On 2020-05-09 15:39:10, user AdamWichura wrote:

How come people in Italy and Spain are vitamin D deficient?

On 2020-06-14 12:52:28, user Nayo57 wrote:

Best recent seroprevalence studies from NYC and Bergamo yield roughly 1500 deaths/100k infections or a crude IFR of 1.5%. With Germany's crude IFR of about 4.5%, the total number of infected would be around 3 times the official estimate. We have to await age-stratified data to refine this estimate.

On the other hand, CFR for medical staff in Germany as reported by RKI is about 0.15% vs 0.2% for age-groups 20-60 years when adjusted to gender-mix in medical staff. This would put the underreported fraction of cases in the range of about 30%.

On 2020-11-25 16:37:17, user Duke Pham wrote:

The main flaws of #solidarity #study can be found here : <br /> https://c19study.com/solida...

HCQ dosage very high as in RECOVERY, 1.6g in the first 24 hours, 9.6g total over 10 days, only 25% less than the high dosage that Borba et al. show greatly increases risk (OR 2.8) [1].

Authors state they do not know the weight or obesity status of patients to analyze toxicity (since they do not adjust dosage based on patient weight, toxicity may be higher in patients of lower weight).

KM curves show a spike in HCQ mortality days 5-7, corresponding to ~90% of the total excess seen at day 28 (a similar spike is seen in the RECOVERY trial).

Almost all excess mortality is from ventilated patients.

Authors refer to a lack of excess mortality in the first few days to suggest a lack of toxicity, but they are ignoring the very long half-life of HCQ and the dosing regimen - much higher levels of HCQ will be reached later. Increased mortality in Borba et al. occurred after 2 days.

An unspecified percentage used the more toxic CQ. No placebo used.<br /> [1] c19study.com/borba.html<br /> death, ?19.0%, p=0.23

According to scientific studies, #hydroxychloroquine is efficient against #covid19. <br /> This website lists all the studies (positive or negative) : www.c19study.com. <br /> Majority of the 181 studies show a reduced #mortality and #severity in the disease with patients treated with #HCQ.

On 2021-03-10 13:52:58, user Jeffrey Brown wrote:

Seems as though an EHR system cannot answer the question posed no matter the inclusion\exclusion criteria. EHRs can only see care within their walls and we know that patients move across providers frequently even in short windows. This means that the look-back period for continuity of care is incomplete and introduces bias, that the look-back for prior conditions is also incomplete, and the outcome data are incompletely captured. Patients often moving across health systems in large cities (example in LA: https://www.ncbi.nlm.nih.go... "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3052345/)"). It is critical to match data to the question, I don't think EHR data can answer the important question posed.

On 2020-05-18 12:43:08, user Sinai Immunol Review Project wrote:

Long period dynamics of viral load and antibodies for SARS-CoV-2 infection: an observational cohort study<br /> Huang et al. medRxiv [@doi.org/10.1101/2020.04.22.20071258]<br /> Main Findings<br /> The presence of serum IgM and IgG against SARS-CoV2 has been shown in several studies, however, a limited number of studies have shown the longitudinal relationship between viral RNA levels and antibody titers. This retrospective, observational study evaluated the dynamics of viral RNA, IgM and IgG specific for SARS-CoV2 proteins in patients with confirmed SARS-CoV-2 pneumonia over an 8-week period. <br /> Throat swabs, sputum, stool and blood samples from 33 patients with laboratory confirmed SARS-CoV-2 pneumonia were collected to analyze viral load and specific IgM and IgG against spike protein (S), spike protein receptor binding domain (RBD), and nucleocapsid (N). The demographics of the patients showed that 24 had respiratory symptom, two had symptoms in both the respiratory and the gastrointestinal tracts, one had gastrointestinal symptoms and six were asymptomatic. Chest CT revealed 27 patients had bilateral infiltrates and six had unilateral infiltrates. All the patients received antiviral treatment and atomized interferon during hospitalization. <br /> While viral load in throat swabs and sputum was higher at the symptom onset and undetectable by three weeks and five weeks respectively, viral load in stool started low but remained detectable for more than five weeks in many patients. The viral loads in sputum declined significantly slower compare to throat, so that the patients were divided into two groups based on load in sputum: short-persistence (viral RNA undetectable within 22 days, n=17) and long-persistence (viral RNA persists more than 22 days, n=16). The relationship between the persistence of sputum viral RNA and antibodies showed that short-persistence group had higher anti-S IgM, anti-RBD IgM and anti-RBD IgG levels compare to long-persistence group suggesting a potential protection by anti-RBD antibodies. The length of time from symptom onset to hospital admission was also associated with SARS-CoV-2 viral clearance. In addition, the higher seropositive rate for anti-S and anti-RBD IgM was seen in long-persistence patients. They suggest that delayed admission to the hospital resulted in higher seropositive and longer infection in patients with COVID-19.<br /> Limitations<br /> The separation of ‘low persistence’ vs ‘high persistence’ groups seems quite arbitrary, as only virus RNA levels for in sputum were considered, and viral loads in throat swabs and stool were not considered (these were no significant difference between the low vs high groups. The manuscript needs better and more detailed description of methods and figure legends. The same color codes for each patient could be used in figure 1, so that the readers could see if there was a trend in viral load between specimens in a same patient, and graphics for each patient will be useful to understand viral dinamics in the three types of samples for each person. The graphs on figure 5 seemed to correspond to one time point data, but there was no explanation which time point was used. In the results section, it was not clear which figures or tables were related to the text. The correlation between severity, viral load and persistency, and antibody titers could be analyzed.<br /> Significance<br /> It is important to understand the relationship between viral loads, disease progression and viral-specific antibodies in COVID-19 disease. More studies are necessary.

Reviewed by Miyo Ota as part of a project by students, postdocs and faculty at the Immunology Institute of the Icahn School of Medicine, Mount Sinai.

On 2025-09-06 14:48:49, user Jeffrey Rothstein wrote:

Nicely done. But I'm surprised you didn't use the appropriate control group when one considers the differential diagnosis of ALS which would include myelopathy, inclusion body myositis, radiculopathy, multifocal motor neuropathy, Thyroid diseas. Controls such as Parkinson's and Alzheimer's any competent neurologist would easily separate from ALS and truly don't add to a diagnostic approach. But mimicking controls would be the most powerful as detailed above. For example, it's likely that muscle markers would also show up in some of those controlled diseases and therefore will be thrown out as providing any kind of disease specificity.

On 2021-12-01 08:32:45, user Wencke wrote:

It seems that all omicron patients coming to Germany were fully vaccinated and PCR tested within 24 hours before the flight. This immune escape correlates to this study:<br /> Increases in COVID-19 are unrelated to levels of vaccination... <br /> https://link.springer.com/a...

On 2020-05-06 18:59:31, user Simonsaid wrote:

What does it mean when you say “Furthermore, there is uncertainty regarding cross reactivity ofSARS-CoV-2 and other coronavirusantibodies.”<br /> Can someone explain please?

On 2022-09-29 18:22:07, user Nikhil Padhye wrote:

Published version can be found here:<br /> Padhye, N. (2022). Bayesian Measurement of Diagnostic Accuracy of the RT-PCR Test for COVID-19. Metrology, 2(4), 414–426. https://doi.org/10.3390/met...

On 2021-03-09 21:34:52, user Marm Kilpatrick wrote:

Thank you for this important study.<br /> Could you please upload all the supplementary materials as a single file? Thanks!

On 2021-03-13 07:48:06, user Dr Gareth Davies (Gruff) wrote:

I noticed that you had previously reported finding a strong correlation but withdrew it. I've studied these data myself and the quality of country data is very poor and inconsistent, so naively applying a regression to it isn't very meaningful.

It's criticially important to use only high quality data sources that as much as is possible represent the nationwide prevelance of deficiency over winter. They should be recent and seasonally adjusted if taken outside winter. Furthermore, the data set should be representative of the entire country.

Each country data set should then be appropriately weighted according to some objective criteria for quality otherwise the regression is meaningless.

Also, very small countries will end up with distorted per million figures, and some effort must be made to ensure that reported figures for deaths and recoveries are accurate since many countries use very different policies. Data for Estonia, Turkey, Czech Repulbic and Boznia and Herzegovina have been added to the regression with apparently equal weighting to other reporting countries despite huge differences in reporting, population densities and data quality for deficiency, mortality and recovery rates.

The data for Czech Republic, for example, is based on Mayer et al. 2012, which cites a study from 2008 of just 560 people which reports 24.4% deficiency. This study was performed over 2–3 months during autumn 2008 - just after summer - and therefore in no way reflects the general population prevelance of vitamin D status in winter in 2020. Indeed, it is wholly inconsistent with other studies which suggest that in Czech Repulic, vitamin D deficiency in winter is widespead (e.g. Bischofova et al. 2018).

It's not surprising that the original clear trend has been wiped out by adding this "dirty data".

The conclusions stated are not merited by the analysis.

On 2021-04-19 11:59:37, user lotrus28 wrote:

Has this study been submitted to a journal?

On 2021-12-23 21:46:48, user Maxime Bedez wrote:

Hello,<br /> At page 4, it is stated that IC50 on Vero cells is 0.038µM and CC50 is 2.9µM. The reference is Fig. 1B. It is not clear, but largely implied by supplementary information, that it is Rodon data (page 7 of Supplementary).<br /> Rodon et al. have published here 10.3389/fphar.2021.646676<br /> In Rodon's paper, the IC50 is 60 and CC50 is 100 (0,06 and 0,1 in nM, page 7).

I am confused, where did I get it wrong ? Did Rodon do another identical experiment with different result ?<br /> I think it need clarification, as 100 and 2900 are really far appart.<br /> Thanks

On 2021-12-31 07:01:37, user Georg Neeby wrote:

Hi, I was surprise to see your paper, it was mentioned in a conspiracy blog, https://childrenshealthdefe...

ITs being used as a reason to not get vaccinated, and for children specifically to not get vaccinated. I took a look at your data, and there is nothing to your paper. Its all just noise, nothing would be reproducible. Your claims massively overstate your data, which basically shows no difference, and you havent controlled for batch effects. Given how this information is being used by nefarious players, you should repeat the entire study with adequate power, I bet none of your new data will show the same trends as your old data.

On 2025-07-25 20:28:33, user Baranger, David wrote:

The final published version of this manuscript is available at: https://www.nature.com/articles/s44220-024-00281-7

On 2020-03-21 08:30:14, user Yuxin Wu wrote:

This study assumes that:

Treatment has minor influence on outcome The provided healthcare in countries is comparable. For developed countries such as Italy and South Korea, it is assumed that the population has similar access to treatment. The death rates reported by age group are thus applicable in all countries.

and then it applies the death rate in one country (South Korea) to other countries. However, the assumption is terribly wrong.

As a matter of fact, the population in different countries/regions of countries have very different access to treatment. In particular, population in areas like Hubei, China and Italy do not have access to as much medical resources as other places since the medical system is overwhelmed.

One evidence. This is what a Lancet report from Italy says about Italy:

Intensive care specialists are already considering denying life-saving care to the sickest and giving priority to those patients most likely to survive when deciding who to provide ventilation to.

Another evidence. Taking today's number, China has a fatality rate of 3139/67800=4.6% in Hubei, but a fatality rate of 122/13639=0.9% outside Hubei.

This false assumption leads to a drastic overestimation of actual cases, in areas that suffer the outbreak the most, namely Iran, China and Italy, shown by Table 2 in this preprint.

On 2021-02-13 17:35:22, user Scott Aberegg wrote:

Where is the supplementary appendix? I would like to see the prior distributions upon which this analysis was based

On 2022-05-24 18:55:47, user Ricardo Durães wrote:

Available at PLoS ONE: https://journals.plos.org/p...

On 2020-05-26 13:58:13, user Sinai Immunol Review Project wrote:

Main findings<br /> While the growing scientific literature on the immune responses to SARS-CoV-2 infection has highlighted several immunological markers for COVID-19, molecular or cellular determinants of disease severity have not yet been well-described. In this report, Sánchez-Cerrillo et al. profiled myeloid and T cell subsets across mild (G1, n=19; whole blood), severe (G2, n=21; whole blood), and critical COVID-19 cases (G3, n=23; whole blood and paired bronchoscopy samples), and healthy controls (n=22). Clinical parameters, including serum IL-6, procalcitonin (PCT), C-reactive protein (CRP), D-dimer levels, and serum LDH, increased with worsening disease severity.<br /> Using high-dimensional flow cytometry, the authors assessed changes in classical monocytes (C Mo; CD14+CD16-), transitional monocytes (T Mo; CD14+CD16+), and non-classical monocytes (NC Mo; CD14loCD16+), CD14-CD16hiHLA-DR- granulocytes, CD141+ dendritic cells (cDC1), CD1c+ dendritic cells (cDC2), and CD123hi dendritic cells (pDC) in blood and bronchoscopy samples. While almost all myeloid subsets in COVID-19 patients were significantly reduced in the blood circulation compared to healthy controls (with the exception of T Mo), no statistically significant correlations between these myeloid subsets and disease severity were observed. Of note, the overall sparsity of C and T Mo subsets corresponded to high levels of serum IL-6; otherwise, there were no remarkable correlations between the frequencies of the aforementioned subsets and inflammatory markers. Importantly, in the bronchoscopy samples, an unpaired analysis identified an enrichment of granulocytes and inflammatory T and NC Mo. Importantly, a paired analysis of blood and lung samples demonstrated that T, NC, and CD1c+ DCs are significantly enriched in the lung. Collectively, these results reflect a notable recruitment of monocytes to the lung. The authors used CD40 expression as a marker of myeloid activation. While CD40 expression decreased with increasing disease severity, this trend was not significant, and expression was comparable to the cells isolated from healthy controls. Lastly, a survey of markers associated with compromised effector function of T cells isolated from blood and bronchoscopy samples of G3 patients showed that CD38+CXCR5+ T cells are significantly more prevalent in the lungs than in the blood, and differences to healthy controls were significant.

Limitations<br /> Technical<br /> One notable limitation are superinfections as a confounding variable; their effects need to be accounted for with careful multi-variate analysis and should be replicated in larger, multicenter studies. Moreover, flow cytometry markers used in the present study can present a biased view of cell populations, so future studies using higher-dimensional, unbiased techniques may provide a more inclusive view of myeloid heterogeneity in COVID-19 patients with differing severities of disease.

Biological<br /> It is important to note that almost all patients across the different groups had been receiving concurrent therapy, including antivirals, antibiotics, steroids, and immuno-modulators (anti-IL-6); it is unclear when these treatments were administered, relative to the collection of samples. Furthermore, the DC subsets defined in this report comprised significantly small proportions (< 5%) of total CD45+ immune cells isolated from blood and bronchoscopy samples of COVID-19 patients. Lastly, while T cell exhaustion was evaluated based on expression of CD38 and CXCR5, the expression of other, more prominent co-inhibitory receptors, including PD-1 or Tim-3, was not evaluated. Therefore, this report would benefit from a better study of myeloid activation and T cell exhaustion using additional markers that define activation of the myeloid subsets, including an analysis of cytokine production, and markers for T cell exhaustion.

Significance<br /> In summary, this report offers some insight into the profiling of different circulating cell subpopulations across various degrees of COVID-19 severity. However, interpretations of the results should be approached with caution, given the lack of statistical significance and of detailed analyses of important cell groups, including better-defined exhausted T cells. However, thus far, the findings outlined in this report support the notion that monocyte dysfunction, involving a pro-inflammatory state and an overall recruitment from the peripheral blood to disease-afflicted tissues like the lung, characterizes the immune response to COVID-19.

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

On 2020-08-25 16:15:15, user kagamiiii wrote:

Should have done leronlimab

On 2020-08-17 18:14:49, user OxImmuno Literature Initiative wrote:

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

On 2024-04-27 20:35:31, user TK wrote:

Wow! Long-overdue research on an important and debilitating condition. Huge thanks to all the researchers investigating!!

On 2020-04-08 10:19:35, user Rosemary TATE wrote:

Hello, thank your for this interesting article.<br /> Could you please upload the relevant checklist. I believe this is PRISMA? I cant see this anywhere. You will need this if you are intending to publish.

On 2023-06-14 10:46:05, user Sayomporn Sirinavin wrote:

The title of the published version was changed by adding a word "nonimmune". <br /> The revised title is:

Effect of Andrographis paniculata treatment for nonimmune patients with early-stage COVID-19 on the prevention of pneumonia: A retrospective cohort study.

On 2020-03-27 20:21:49, user Jessa Elizabeth wrote:

Yes but out of all those test how many tested positive with a RH -. I ask bc my bf has it, A+, I have A- and did not get it, living in the same house. My daughter is O- and did not get it either. My dad has it, A+, and my friends husband has it A+ both infected but the wife is A- like me and didn't catch it. Just curious on if that plays a part?

On 2021-09-26 18:18:34, user wolvverinepld wrote:

How long was the period from the second dose to the study?

Pfizer study (Qatar)

Asymptomatic infection protection<br /> Highest 63.7% at 0-4 weeks<br /> 0% by 15 weeks

Symptomatic<br /> 49.6% at 15 weeks<br /> 0% by 20 weeks

https://www.medrxiv.org/con...

On 2021-12-05 07:06:49, user Robert Thompson wrote:

This is another paper with undisclosed PCR Ct values. Diagnostic confidence is thus limited. There should also be some discussion of the kinetics of the serology tests- Nucleocapsid antibodies decay over time. There were a high number (12 of 20) apparently asymptomatic infections, but due to the assays used it would be difficult to identify those who had previous infection and recovery. As well, there is a time function, both seasonal and position in the epidemic wave, which complicates the analysis. A similar geographic uncertainty exists, as the timing of wave peaks varied through 2020 from region to region.

On 2020-05-22 15:28:22, user K N wrote:

Can anyone comment on this sentence: <br /> "The age dependent IFR range from below 0.04% for ages below<br /> 50 years to 2.53%, 7.12%, and17.5% for ages 70-79, 80-89, and above 90 years,<br /> respectively, (Table2)." Is there a reason why ages 50-69 seem to be excluded?

On 2020-04-04 22:53:46, user Dick Stern wrote:

I believe these forecasts are terribly deceiving! The death tolls the projections in Florida for example seem incredibly underreported. Even in the best case of all assumptions Florida could have death tolls of over 100,000. They have not accepted social distancing, are not staying home,: they are not flattening the curve. With the number of seniors over 65 at approximately 4,465,169 this is a disaster waiting to happen.<br /> The death toll for people over 65 exposed to the Coronavirus Sars 2 is around 8%. That means if half the population of the elderly must be exposed to Covid-19 before herd immunity starts to kick in. <br /> Then the death toll in just this age group could be 176,000 or more. Alternatively, a very conservative death rate is 1% of the general population of over 21 million would lead you to believe that there will be 210,000 deaths!<br /> I also don't see a cumulative nature of ventilator usage. A patient must stay on a ventilator for several days. It can be as long as 15 days. How come the ventilation equipment usage curve is growing slowly. In fact you will not kick someone off ventilators until after the 5 to 15 days of usage. The growth of the ventilators required should be be closer to a logarithmic growth curve and then flatting at the limit of number of ventilation tubes available.

On 2020-05-08 14:37:27, user Merilee Brockway, PhD RN IBCLC wrote:

I think that you need to consider the possibility of retrograde flow contaminating the breastmilk from the infant's saliva. Sicker infants would likely have a higher viral load in their saliva/respiratory secretions. A study in the Lancet found that "The mean viral load of severe cases was around 60 times higher than that of mild cases, suggesting that higher viral loads might be associated with severe clinical outcomes." https://www.thelancet.com/j.... This may help to explain why the virus was present in the milk of mother 2, but not mother 1. Infant 2 was much sicker than infant 1 and as such the viral load was likely much higher.

On 2024-07-09 12:41:39, user Peter A McCullough wrote:

Binkhorst and Goldstein have used a small sample size which is insufficient to find the signal of COVID-19 vaccination, subclinical myocarditis, and sudden death in athletes triggered by catecholamines during exertion. In June 2021 the US FDA and CDC issued a warning on mRNA COVID-19 vaccines and myocarditis as a serious adverse event. Binkhorst and Daniels are advised to be cautious and conservative on new genetic biotechnology that has clear cardiac safety concerns in the published literature and by regulatory authorities.

We have found it takes a vaccinated population of ~2 million to readily observe the vaccine effect of increasing cardiac arrests. See Hulscher, N.; Cook, M.; Stricker, R.; McCullough, P. A. Excess Cardiopulmonary Arrest and Mortality after COVID-19 Vaccination in King County, Washington. Preprints 2024, 2024051665. https://doi.org/10.20944/pr...

https://www.preprints.org/m...

On 2020-05-30 18:13:16, user Sam Wheeler wrote:

What's the result for different types of masks? Surgical mask, FFP3 mask, FFP2 = KN95 = N95 mask? The most well known brands like 3M, vs. unknown brands?

On 2020-07-03 09:19:51, user Lolo229 wrote:

Do these findings suggest that people with severe food allergies are more at risk for ventilation if they were to contract COVID-19?

On 2021-06-30 13:49:14, user Toksyuryel wrote:

Conclusion is poorly-worded. This study only looked into the potential for re-infection and the conclusion should reflect that. There are other studied benefits to vaccinating previously infected individuals and you should not imply to invalidate those with a study that looked into none of those benefits.

On 2022-01-16 16:31:04, user holder66 wrote:

Article is now published; pubmed pmid 35028662

On 2020-05-07 14:01:03, user Dr Gareth Davies (Gruff) wrote:

Please note: the current version on medRxiv is an intial draft. A newer draft is being submitted soon with some important improvements and clarifications so we request everyone to please hold off on critiquing until the final draft is preprint submission is approved so that we don't waste time responding to issues that have already been addressed since draft 1.0. Many thanks!

On 2023-03-09 12:14:10, user Guido van Wingen wrote:

Great study showing that high quality multimodal MRI data does not improve classification performance beyond multicenter resting-state fMRI as reported for two other large cohorts (REST-meta-MDD with N=2338 and PsyMRI with N=1039): https://www.nature.com/arti...

On 2021-04-16 16:04:08, user Dirk Van Essendelft wrote:

Just curious about the age distribution. The FE vaccinated cohort appears to be significantly older than any other cohort and also exhibits the highest B.1.351 infection rate. Is it fair to conclude that the vaccine is less effective against this strain or is it fair to conclude that the B.1.135 strain is more infectious for an elderly population.

On 2021-08-26 14:47:37, user bbeaird wrote:

The science looks solid. I think the challenge is how to interpret the findings. I did expect antibody concentrations to decline over time, in both vaccinated and convalescent populations. The 'aha moment' revolves around the difference in decay rates. But...my interpretation is not that people should avoid vaccination. The penalty of death or serious illness is too great. Nor can you expect people to take booster shots annually forever. I believe the path out of this misery is to get vaccinated, and then subsequently most vaccinated people will still contract the virus, though the effects will be minimal as compared to being unvaccinated and getting sick. Thus, the vaccination provides a safe bridge to a level of antibodies for which the decay rate is much more gradual and sustainable. One more comment...I believe there is an error in the text, on the percent of vaccinated people who have antibody concentrations below the minimum protection level, listed as 5.8% at 3 months. Yet the accompanying graph shows 5.8% at 1 month and 9.2% at 3 months. This error doesn't change the findings. Just a friendly note that the figures should be changed to match.

On 2020-03-24 22:52:54, user Sinai Immunol Review Project wrote:

Title: Clinical findings in critically ill patients infected with SARS-CoV-2 in Guangdong Province, China: a multi-center, retrospective, observational study?<br /> Immunology keywords: clinical outcomes, prognosis, critically ill patients, ICU, lymphopenia, LDH

Main findings: <br /> This work analyses laboratory and clinical data from 45 patients treated in the in ICU in a single province in China. Overall, 44% of the patients were intubated within 3 days of ICU admission with only 1 death.<br /> Lymphopenia was noted in 91% of patient with an inverse correlation with LDH. <br /> Lymphocyte levels are negatively correlated with Sequential Organ Failure Assessment (SOFA) score (clinical score, the higher the more critical state), LDH levels are positively correlated to SOFA score. Overall, older patients (>60yo), with high SOFA score, high LDH levels and low lymphocytes levels at ICU admission are at higher risk of intubation.<br /> Of note, convalescent plasma was administered to 6 patients but due to limited sample size no conclusion can be made.

Limitation of the study: While the study offers important insights into disease course and clinical lab correlates of outcome, the cohort is relatively small and is likely skewed towards a less-severe population compared to other ICU reports given the outcomes observed. Analysis of laboratory values and predictors of outcomes in larger cohorts will be important to make triage and treatment decisions. As with many retrospective analyses, pre-infection data is limited and thus it is not possible to understand whether lymphopenia was secondary to underlying comorbidities or infection. <br /> Well-designed studies are necessary to evaluate the effect of convalescent plasma administration.

Relevance: This clinical data enables the identification of at-risk patients and gives guidance for research for treatment options. Indeed, further work is needed to better understand the causes of the lymphopenia and its correlation with outcome.

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

On 2020-07-14 07:00:20, user Nico las wrote:

line 97:78.5% of males<br /> lines 137 - 139: it would be safer to make a statistical test to control for poolability of individual data series before making a group regression.<br /> Great job at collecting and analyzing data.

On 2020-07-13 22:41:50, user Jim Coote wrote:

I share the concerns expressed in the previous 2 comments. Surely the decrease in antibody levels would be entirely expected after the primary response. The acid test would surely be whether there was a good secondary response to any Covid19 based antigen. Any analysis of that should examine the cell based response as well as the humoral.

Considering the concerns likely to be raised by their findings, I think it is a serious omission not to compare the data to antibody levels typically seen following primary responses to infections on which we have solid information on long term immunity, (both weak and strong). However this would be a completely academic consideration provided a good secondary response to Covid 19 antigen / virus was seen.

On 2020-08-20 20:15:56, user scvblwxq wrote:

B-Cells should still be available to generate new antibodies if needed.

The antibodies are being used to estimate how many people have been infected in total. That count will be low if people's antibodies become undetectable before they are tested.

On 2021-07-23 11:43:39, user andyround wrote:

Fascinating, thanks. What I can’t square between studies like yours and the one on cynomolgus monkeys on the one hand, and the range of estimates of sizes of droplets in respiratory exhalations on the other (as recently reviewed by Lydia Bourouiba for example), is how the quantity of viral RNA apparently scales with the *number* of droplets rather than their volume. It implies that the concentration of viruses per droplet is hugely dependent on the size of the droplet and I can’t think of a mechanism to achieve this - are viruses massively self-repelling? (over micron-scale distances?) Are they highly surface active? I wonder if you have thought about this.

On 2021-05-26 07:10:41, user Robert Clark wrote:

To the authors: with millions of lives at stake, you do not want to be on the wrong side of history on this.

The most ethical response considering the extreme importance of the issue is to go beyond just retracting and actually rewrite to conclude IVM by best available evidence does appear to have effectiveness as a treatment for COVID.

Robert Clark

On 2021-04-20 02:03:34, user Hector Moises Chip / Micro Chi wrote:

By "reasoning" - that is according to Kant's a priori approach - to keep schools open would be a source of virus transmission. Basically because in spite of gathering "in bubbles", it breaks the gold epidemiologic principle of social distancing, particularly difficult in youngsters besides the fact that they wander (usually) in several unchecked other bubbles... Also there are on the empiric side, cases of intra school viral circulation that the present article has not searched . The whole script is therefore incomplete enough to draw firm conclusions. In any case, it would mean to stay in the prudent side, which is do not open school if the sanitary system is on crisis.

On 2020-09-07 03:47:09, user Stephen D wrote:

Your conclusion is faulty. Note that nothing in your data implies that anything should be made "mandatory". Your modeling might imply that if everyone wore a mask 24/7, the effect would be to reduce the probability of a certain increase in infections. But it cannot in principle have any implication as regards legal responses by governments. This is not science. Your conclusion is framed using political and ethical concepts implied in the term "mandatory" that are in principle not amenable to science, and cannot be inferred from data or models.

On 2019-07-21 06:26:16, user Guyguy wrote:

ENGLISH

OFFICIAL PRESS RELEASE RELATED TO THE EPIDEMIC OF EBOLA VIRUS DISEASE IN EASTERN DRC

1. The Democratic Republic of the Congo takes note of the statement by the World Health Organization (WHO) that the current epidemic is a public health emergency of international concern and endorses the recommendations of the WHO Director-General not to impose travel and trade restrictions and stigmatization of populations already in need of assistance.

2. The Democratic Republic of the Congo reiterates its strong commitment to continue the response to the Ebola virus epidemic and to strengthen cross-border control and control of major internal roads to ensure that no cases are omitted or escapes from the surveillance teams.

3. The response to the Ebola Virus Disease outbreak is now under the direct supervision of His Excellency the President of the Republic. To this end, it was decided to entrust the responsibility of the Technical Secretariat of the Multisectoral Committee to a team of experts under the direction of Professor Jean Jacques MUYEMBE TAMFUM.

4. This team of experts is responsible for coordinating all the activities for implementing the Ebola response strategy. The Technical Secretariat is in charge of putting in place all the innovative measures that are urgent and indispensable for the rapid control of the epidemic.

5. His Excellency the President of the Republic reassures the Congolese people and the neighboring countries that the measures currently taken in connection with the response to the Ebola Virus Disease in the DRC are likely to eradicate this epidemic.

Kinshasa, July 20th, 2019.

Source: Office of the President of the Democratic Republic of the Congo

********************************<br /> FRENCH

COMMUNIQUE OFFICIEL EN RAPPORT AVEC L'EPIDEMIE DE LA MALADIE A VIRUS EBOLA A L'EST DE LA RDC

1. La République Démocratique du Congo prend acte de la déclaration de l'Organisation Mondiale de la Santé (OMS) faisant de l'épidémie actuelle une urgence de santé publique de portée internationale et fait siennes les recommandations du Directeur Général de l'OMS de ne pas imposer des restrictions des voyages et de commerce ainsi que la stigmatisation des populations se trouvant déjà dans le besoin d'une assistance.

2. La République Démocratique du Congo réitère son ferme engagement à poursuivre la riposte à l'épidémie de la Maladie à virus Ebola et à renforcer le contrôle transfrontalier et celui des principales routes internes afin de veiller à ce qu'aucun cas ne soit omis ou n'échappe aux équipes de surveillance.

3. La conduite de la riposte à l'épidémie de la Maladie à virus Ebola se fait désormais sous la supervision directe de Son Excellence Monsieur le Président de la République. A cet effet, il est décidé de confier la responsabilité du Secrétariat Technique du Comité Multisectoriel à une équipe d'experts, sous la direction du Professeur Jean Jacques MUYEMBE TAMFUM.

4. Cette équipe d'experts a pour mission d'assurer la coordination de l'ensemble des activités de mise en oeuvre de la stratégie de riposte à la Maladie à virus Ebola. Le Secrétariat Technique est chargé de mettre en place toutes les mesures innovantes urgentes et indispensables au contrôle rapide de l'épidémie.

5. Son Excellence Monsieur le Président de la République rassure les populations congolaises et les pays voisins que les mesures actuellement prises en rapport avec la riposte à la Maladie à virus Ebola en RDC sont de nature à éradiquer cette épidémie.

Fait à Kinshasa, le 20 juillet 2019.

Source: Cabinet du Président de la République Démocratique du Congo

On 2020-04-23 14:14:16, user Pasquale Valente wrote:

How was the case of pneumonia defined?<br /> How was the causal link with SARS CoV-2 demonstrated?

On 2020-05-03 13:39:59, user Cristine Carrier wrote:

Wow, I can't believe they made almost the exact same mistake as the doctors in Bakersfield. On what planet would people actively seeking out medical care a representative or random sample of the entire population of a city? If they had 33 cases of broken legs would they then use that number to calculate that the entire city of Kobe had the same rate of broken legs as the people going to the clinic?

On 2022-01-27 21:22:51, user Michael Klar wrote:

They have NOT done their homework:

This investigation uses no suitable surrugate for human aerosols. These consist mostly of mucin5 and this is a hydrogel. Hydrogels behave differently than the one used Serum. This is reflected in the Shrinkage factor of 2.5 versus 4-5 in humans.

The results of the preprint should not be evaluated, as another previously published study shows that the liquid composition is crucial for the inactivation rate:

https://www.pnas.org/conten...

On 2021-06-12 06:21:09, user Maksim wrote:

By now the manuscript has been reviewed by three reviewers in two different journals. Opinion of one reviewer is mostly positive, two reviewers are very skeptical regarding methodological approach (per se) used in the manuscript. Regarding this skepticism I would like to mention that while ecological studies do have limitations, these are considered as useful and widely used in the field, in particular in relation to COVD-19 (e.g., Escobar et al., 2020 PNAS, https://www.pnas.org/conten... Urashima et al., 2020 IJERPH https://www.mdpi.com/1660-4... "https://www.mdpi.com/1660-4601/17/15/5589)").

On 2021-07-31 00:05:48, user Arthur wrote:

Check these stats from results section.<br /> The percentages of white, black and Latino participants do not add up to 100%.

Please check before publishing , these are some things that makes a publication lose credibility.

Participants were 49% female, 82% White, 10% Black/African American, and 26% Hispanic/Latinx; median age was 51 years.

Then

Of vaccinated participants, 58% had >=2 months follow-up post-dose 2, 49% were female, 86% were White, 4.6% were Black/African American, and 12% were Hispanic/Latinx.

On 2021-08-01 14:47:19, user Nir Tsabar wrote:

In the 'Disposition of Participants' chart, the numbers of participants who 'Entered open-label follow up' (lowest items) and those of 'Withdrawal after Dose 2' do not add up to those 'Received Dose 2'. <br /> There seem to be missing 583 participants in the Placebo group and 1258 in the Pfizer BNT162b2 group.<br /> Moreover, a clear statement regarding the possibility of unknown deaths in the randomized groups may be very important.

On 2021-08-05 17:53:36, user pedro paulo castro wrote:

It doesn't seem right that a much lower number of subjects from the vaccinated group came down with COVID 19, but the same number died as in the placebo group, which seems to indicate therefore a higher proportion of deaths among those who contracted COVID 19 AND were vaccinated. There is a conspicuous lack of what would have been a very useful breakdown of the instances of death, in such a way that we could see, for both groups, what number of deaths was among those who had COVID or those who didn't have COVID. This prevents us from seeing whether a subject had COVID, but had his or her death reported as, say, cardiac arrest, for example, which might change the context a bit.

On 2021-03-20 14:23:19, user Alexander Mathioudakis wrote:

This study has now been published here:

https://www.mdpi.com/2075-1...

On 2020-09-16 19:31:28, user Ibrahim Hussin wrote:

I believe the precipitation in the weather type of Drizzle has effect on the outbreak

On 2025-07-13 08:45:42, user Ben Auxier wrote:

In their pre-print Brackin et al. [1] present data suggesting nosocomial infections (that is, infections arising from the clinical environment) of patients infected with A. fumigatus. This is a surprising finding, given the near universal abundance of this fungus. As I detail below, there is no evidence of transmission chains within a hospital. Rather, the analyses presented fall victim to the statistics of detecting matches within populations of differing sizes, related to what is commonly referred to as “the birthday paradox”. The main data in this paper consists of whole genome sequencing data from 182 isolates from 15 patients (>2 samples from each patient), 101 isolates from patient’s homes, and 102 isolates from a medical centre that all patients visited. From these data, three comparisons are made between a) case samples and general environmental samples, b) case samples and their own home and c) case samples and the reference clinic.

The authors find that there are links for a), consistent with reports over the last several decades that A. fumigatus populations are highly recombinant, but includes widely dispersed clones [2–5]. More interestingly, they find no links for b) but abundant links in c), which would be consistent with hospital spread. However, while the sample sizes in b) and c) are equivalent, the comparisons are not. Across the 8 cases (average of 11.3 isolates per case) where the housing was also sampled, an average of 12.6 isolates per house (101 total) were used for whole genome sequencing. This leads to ~1000 comparisons being made, due to substructure in the data. Notably, since some patients have long-term infections of one genotype, this number is an overestimate due to within-patient correlations. Then, all 182 patient isolates (more than the 8 patients sampled) are compared against all 102 isolates from the medical centre, producing over 18,000 comparisons. Thus, using a null hypothesis of no difference between patient-hospital and patient-home data, since there are ~20X more patient-hospital comparisons (and 20% of patient samples match a hospital sample), a naïve expectation would be 1% of patient-home comparisons to be clonally related, likely detectable in the ~1000 comparisons.

Unfortunately, their analysis falls into the “birthday paradox”. Briefly stated, this paradox reflects the fact that while the chance that you share a birthday with someone else is 1/365, the chance that two people share a birthday within a classroom of 30 students is not 8% (30/365), but instead a surprisingly high 70%. This is because in the classroom situation you not only have a larger group, but also many more combinations. The chance of sharing a birthday can be considered as the chance of sampling two identical genotypes from a population of clones. Thus, while roughly equal numbers of isolates from homes and the reference center were used for genome sequencing, this difference in structure means that comparisons with patient isolates are unequal. However, the birthday paradox shows that this math is not intuitive and the chance of finding matches increases non-linearly. So, while perhaps 10 matches should have been expected between patients and their homes, which would already be a tenuous link, the expected number is effectively zero due to the smaller sample size.

The actual sites of infection for A. fumigatus is important to discern. The cryptic nature of initial infections makes this a challenging task, requiring creative experimental or observational studies. However, I would argue simply identifying clonal matches provides insufficient evidence..

References:<br /> 1. Brackin, A. P. et al. Genomic epidemiology links azole-resistant Aspergillus fumigatus hospital bioaerosols to chronic respiratory aspergillosis. 2025.07.04.25330042 Preprint at https://doi.org/10.1101/2025.07.04.25330042 (2025).

1. Chazalet, V. et al. Molecular Typing of Environmental and Patient Isolates of Aspergillus fumigatus from Various Hospital Settings. Journal of Clinical Microbiology 36, 1494–1500 (1998).

2. Rhodes, J. et al. Population genomics confirms acquisition of drug-resistant Aspergillus fumigatus infection by humans from the environment. Nat Microbiol 7, 663–674 (2022).

3. Shelton, J. M. G. et al. Landscape-scale exposure to multiazole-resistant Aspergillus fumigatus bioaerosols. 2022.11.07.515445 Preprint at https://doi.org/10.1101/2022.11.07.515445 (2022).

4. Snelders, E. et al. Widely dispersed clonal expansion of multi-fungicide-resistant Aspergillus fumigatus limits genomic epidemiology prospects. mBio 16, e03652-24 (2025).

On 2024-02-28 20:15:40, user Robert Chambers' vestiges wrote:

Great paper especially the common detection. in cases of encephalitis. Also nicely list past reports of these viruses in diverse systems.

Could it be that these gemykibivirus actually infect some unidentified protozoa that is actually causing the disease?Many other CRESS-DNA viral genomes seem to infect protozoa as reported in https://pubmed.ncbi.nlm.nih...<br /> https://www.mdpi.com/1422-0...

On 2020-04-22 23:23:26, user Eric Solrain wrote:

"It was also reported that the maximum outdoor air supply was operated during the quarantine<br /> period." Is this 100% fresh air with no return? The referenced article (https://www.jstage.jst.go.j... ) notes that 100% fresh air is the norm, but for energy efficiency cabins are reduced to 30%. Full economizer mode (at 100% fresh air) is also a common energy saving measure.

On 2020-05-20 13:11:39, user Raquel Rabionet wrote:

Hi, nice work.

it's interesting that there is such a clear difference in methylation of a single CpG between the V30M carriers and those of other variants in TTR gene. Have you considered that this V30M variant that is so highly associated to the cg13139646 site (located in TTR exonic region) is really close to this site? Based on your table, the cg site is at chr18:29172936, while the V30M variant is at chr18:27172937, just one base pair away. I wonder if there might be some kind of interference with the detection?

If so, maybe you could confirm the methylation at this site using other methods?

On 2020-10-24 02:24:38, user Elena wrote:

Dear author,

After reading your article, here are my comments. I will start out with positive; the title was great. It was straight to the point and exactly told what this paper is about. I like how it is broken down to individual parts in the abstract. It helped me navigate that section better. Your explanation of what studies were performed before were helpful. There were a couple of items that were missing. For example, why you chose peanuts and not of any of the other common allergens were missing. Also, in your methods, you said that you chose 3 families to get 2.5 or 5 grams and never explained why you chose 3 families and what that was for especially when all of the other families were feeding their infants one gram. I also feel that the methods and the results weren't well-organized. I feel like if you just reorganized those sections the paper would flow better.

On 2021-10-26 21:25:43, user Eugene Peskin wrote:

The article doesn't provide much clarity how the number of cases among the non-immune was actually calculated.<br /> If accomodation for immune layer of 46% has been done to re-calculate attack rate for control group, it should also be accomodated for the main group calculation, as 46% one-time vaccinated already had immunity before vaccination (actually less, you should deduct those who got their immunity from previous vaccination).

On 2021-12-30 21:07:17, user madmathemagician wrote:

Apart from using COVID-19 related data, it has no relevance to the field of medical, clinical, and related health sciences. It does not belong on medrxiv.org.

On 2021-04-27 03:16:13, user vijayaddanki wrote:

Very interesting paper. Once you identified the mutations and found that these are unique variants, how did you determine the parent lineage? Did you use any programming tools or did you manually identify the parent lineage. I have a set of new unique variants (with a detailed list of mutations in the Spike protein), their GISAID Accession IDs, origin dates/locations and current dates/locations where it is prevalent. But I am very confused on how to submit it to get a new Pangolin lineage designation.

On 2022-01-16 09:33:16, user Joel Green wrote:

Can the authors please clarify my understanding of their data, because it doesn't appear to make sense to me.

The authors calculations appear to state that in a home inhabited by 5 people, and 1 person is infected, that 18 people need to be excluded from the home in order to prevent Sars-Cov-2 transmission within that home?

Easy example to follow using the graphs in the paper:<br /> - Page 15, Household Graph, third from left<br /> - 20% baseline infection risk, NNE = approximately 18.<br /> - From Page 6: Baseline infection risk "is the current point-prevalence of infectious cases"<br /> - From Page 2: "excluding unvaccinated people to reduce transmissions is described, called the number needed to exclude (NNE)"

Applying those numbers:<br /> - A household of 5 unvaccinated people, 1 of whom is infected<br /> - This represents a baseline infection risk of 20%<br /> - According to the graph on page 15, and according to the TITLE of this paper:<br /> "The number of unvaccinated people needed to exclude to prevent SARS-CoV-2 transmissions" = 18

Q1: Can the authors explain why their research shows that 18 people need to be excluded from a home that only contains 5 people in order to prevent Sars-Cov-2 transmission where one person in the home is already infected?

Q2: Will the authors address the valid questions raised by others in these comments and explain exactly what an "event" comprises of?

Q3: Why do the authors believe that calculating the NNE from 1 single event, one time only, be used to draw a conclusion about the benefits of isolation over the course of several months? It is clear that the unvaccinated would be be excluded from several events over the course of a covid wave but I'm not sure where they have come up with a cumulative figure.

On 2021-12-04 00:21:53, user TaShelby wrote:

These results are important and are consistent with findings in “Quantitative SARS-CoV-2 viral-load curves in paired saliva and nasal swabs inform appropriate respiratory sampling site and analytical test sensitivity required for earliest viral detection.” Doi:10.1101/2021.04.02.21254771. See https://www.medrxiv.org/con...

On 2020-07-19 10:40:10, user vsn74 wrote:

1st of July: <br /> - 5.497 covid deaths<br /> - 50,266 deaths (all causes)<br /> That was a HUGE MISTAKE, you guys did!

On 2020-05-06 08:05:15, user Prof Pranab Kumar Bhattacharya wrote:

Dear Editor<br /> In the world, Corona virus cases jumped up till 3rd May 2020 from December 2019 is 3,51,743 with death 2,45,617 (18%) and 31.5 death per one million people of infected.Almost 212 countries worldwide and most affected countries are USA,( death rate 304, followed by Spain (540),Itali 475, UK 414, France 379 per million population when in India total cases of positive by RT PCR is 40,266 death 1300 per one million people and in West Bengal province of India total infected is 963 with death 48 cases as per ministry of health government of India records on covid 19. The question is why such a huge percentage of death from this dangerous virus ( no more should be considered simple like influenza virus) inspite of lockdown, social distancing ventilation guided treatment protocol for mild moderate and severe pneumonia from covid 19?<br /> Mortality from covid 19 is higher in groups at higher risks of thromboembolism including hypertension, types 2DM, obesity, coronary artery disease ,cardiomyopathy, pre existing renal pathology as co morbid condition known to all. It has been also seen world wide that the risk of thromboembolism ( both venous and arterial) are more likely to occur when patients are admitted at ICU or in PEP ventilation, ànd in aged over 60 yrs( approximately 63% of death in India from covid 19).<br /> What did the autopsy studies revealed of these death, though very limited autopsy were performed with covid 19 death as the virus is HG 3 category virus. Brane Hanely (1) eral published in journal of clinical pathology of BMJ group showed histopathology of lungs on HE stain oedema, Type Ii pneumocytes hyperplasia,large pneumocytes with ground glass viral inclusions bodies focal inflammation, multinucleated giant cells,when no hyaline membrane ( a histopathological features of ARDS) diffuse alveolar damage. The pulmonary vessels showed hyaline necrosis with thrombus formation and capillary congestion.inflamatory infiltrate composed of alveolar macrophages in alveolar lumen and lymphocytes in interstitium. Zhe Xu et Al (2) in journal Lancet reported also one 50 year old man died on day 14 of covid 19 after being treated with lopinovir+retinovir+moxiflixain and high nasal cannula oxygen therapy and niddle autopsy of lungs liver and heart tissue showed diffuse alveolar damage with cellular fibrimyxiod exudate,dissquamation of pneumocytes and hyaline membrane formation (sign of ARDS) , interstitial mononuclear inflammatory infiltrate dominated by lymphocytes ( CD8) multi nucleated syncitial giant cells, atypical pneumocytes and microvascular thrombosis in pulmonary vessels (2).Sufang Tian et Al (3) did post mortem needle core autopsy of four patients who died of severe covid 19 pneumonia and patients age range were 59-81 years and time of death 15-52 days were in ventilation. Histology of their finding in lungs were again diffuse injury to alveolar epithelial cells, hyaline membrane formation, hyperplasia of type II pneumocytes , diffuse alveolar damage and consolidation by fibroblasts proliferation with extra cellular fibrin forming clusters.All these tour cases had vascular congestion with intravascular thrombus suggesting an acute phase components reaction and fibrinoid necrosis of blood vessels.The autopsy finding of heart was that endocardia and myocardia didn't contain inflammatory cellular infiltrate, although focally myocardium appeared irregular in shape with darkened cytoplasm and fibrinoid necrosis of blood vessels in myocardia.There were various degrees of focal oedema interstitial fibrosis and myocardial hypertrophy which suggests patients had underlying hypertension associated with hypertrophy or past ischemic injury. A large series of 38 cases of autopsy of lung by Luca carsana etall (5) showed from death cases of covid 19 in northern Itali on H&E stain showed also diffuse alveolar damage, capillary congratulations, necrosis, necrosis of pneumocytes, hyaline membrane, interstitial oedema,type II pneumocytes hyperplasia, platelet fibrin rich thrombus(5) .Electron microscopy showed viral particles within cytoplasmic vaccoule of pneumocytes.<br /> So from above post mortem studies, besides ARDS like pictures in terminal event , platelet fibrin rich thrombosis of pulmonary vessels, myocardial vessels, hyaline necrosis of blood vessels of both lungs and of myocardium are prominent picture along with endothelial dysfunction according to this author.The severe cases of pneumonia from covid 19 also shows increased D Dimer value (4) prognostically bad , increased c reactive protein, increased pro calcitonin and increased FDP value<br /> All these suggest to me that pathogenesis behind so many death in ventilation or at ICU of covid 19 patients are not ARDS itself but some kinds of coagulopathy or DIC occurred before death in severe pneumonia cases<br /> Though lymphopenia, inflammatory cytokine stroms ( raised IL6,raised TNF are for cytokine stroms)are typical abnormalities described in almost all literature in highly pathogenic Covid 19 infection with disease severity ,only one rapid response in BMJ (4) suggest , based on post mortem finding use of low molecular weight heparin (LMWH) to be included in the treatment modules of covid 19, particularly those who have high D Dimer high FDP value in serum though TT,APTT,PT,INR may not show any significant difference.use of heparin therapy with constant monitoring for bleeding manifestation should be instituted in patients showing clinical signs of turning towards severe pneumonia,along with antiviral therapy with remdesvir (within 7 days onset of symptoms at scheduled disease)<br /> If the pathology behind the death of severe pneumonia in covid 19 patients is DIC ( according to Autopsy finding the pneumocytes are not killed or destroyed by the virus nor by cytotoxic T cells, rather proliferation occur with much viral replication and virus load) there will be DIC , vascular congestion, thrombosis there will be AMI stroke ) then treatment at ICU with ventilation become useless unless if thromboembolism is not resolved first with LMWH infusion <br /> Referencs <br /> 1) Brain Hanley, Sebastian B Lucas,Esther youd,Benjamin swift,Michael Asbron "Autopsy in suspected covid 19 cases " JCP 73,(5):2020 http://dx.doi.org.10.1136/jclinpath-2020-20652<br /> 2) Xu Z,Shi L,Wang y eral "Pathological finding of covid 19 associated with acute respiratory distress syndrome " The Lancet respiratory medicine 8 (4):420-22 :2020<br /> 3) Sudan Tian, young xiong,Shu yuan xiao,Liu H et all "Study of 2019 novel Corona virus disease ( covid 19) through post mortem core biopsy" Modern pathology (Nature.com ) 14 th April 2020 http://doi.org/10.1038/s 41379-020-0536-<br /> 4) William Atenio ,Nadu Okonkwo "should prognostic models for covid 19 not also incorporate markers of thrombosis" Rapid Response published BMJ on 14th April 2020 to article"Prediction model for diagnosis and prognosis of covid 19 infection: systematic Review and clinical analysis" The BMJ 2020:369:m1328 published on 7th April 2020 https://doi.org/10.1136/bmj...<br /> 5)Luca carsana, Aurelo sanzogoni ,Ahmed Nast, Roberta Rossi etall"pulmonary post mortem finding in a large series of covid 19 cases from northern Itali" MedRxiv https://doi.org/1101/2020.0...

On 2021-11-09 21:39:32, user Andy Bloch wrote:

Conclusions are contradicted by this paper: Waning of SARS-CoV-2 antibodies targeting the Spike protein in individuals post second dose of ChAdOx1 and BNT162b2 COVID-19 vaccines and risk of breakthrough infections: analysis of the Virus Watch community cohort.

On 2022-02-03 18:10:45, user Rodrigo Zepeda wrote:

Methods equation 6. Y(t) is never defined. Is it the observed case count?

On 2021-10-04 06:59:17, user kdrl nakle wrote:

EMT, does not surprise me. Too bad this is before Delta.

On 2021-06-06 07:02:22, user Ju-Sheng Zheng wrote:

This work is now published in the Journal of Genetics and Genomics. 2021. doi: 10.1016/j.jgg.2021.04.002

On 2020-04-23 17:27:44, user Sinai Immunol Review Project wrote:

Presence of SARS-CoV-2 reactive T cells in COVID-19 patients and healthy donors

Braun J et al.; medRxiv 2020.04.17.20061440; https://doi.org/10.1101/202...

Keywords

• SARS-CoV-2 specific CD4 T cells

• Human endemic coronaviruses

• COVID-19

Main findings

In this preprint, Braun et al. report quantification of virus-specific CD4 T cells in 18 patients with mild, severe and critical COVID-19, including 10 patients admitted to ICU. Performing in vitro stimulation of PBMCs with two sets of overlapping SARS-CoV-2 peptide pools – the S I pool spanning the N-terminal region (aa 1-643) of the S protein, including 21 predicted SARS-CoV-1 MHC-II epitopes, and the C-terminal S II pool (aa 633-1273) containing 13 predicted SARS-CoV-1 MHC-II epitopes – the authors detected S-protein-specific CD4 T cells in up to 83% of COVID-19 patients based on intracellular 4-1BB (CD137) and CD40L (CD154) induction. Notably, peptide pool S II shares higher homology with human endemic coronaviruses (hCoVs) 229E, NL63, OC43, and HKU1 that may cause the common cold, but it does not include the SARS-CoV-2 receptor-binding domain (RBD), which has been identified as a critical target of neutralizing antibodies in both SARS-CoV-1 and SARS-CoV-2. S I-reactive CD4 T cells were found in 12 out of 18 (67%) patients, whereas CD4 T cells against S II were detected in 15 patients (83%). Intriguingly, S-specific CD4 T cells could also be found in 34% (n=23) of 68 SARS-CoV-2 seronegative donors, referred to as reactive healthy donors (RHD), with a preference for S II over S I epitopes. Only 6 of 23 RHDs also had detectable frequencies of S I-specific CD4 T cells, overall suggesting S II-reactive CD4 T cells had likely developed in response to prior infections with hCoVs. Of 18 out of 68 total healthy donors tested, all were found to have anti-hCoV antibodies, although this was independent of concomitant anti-S II CD4 T cell frequencies detected. This finding mirrors observations of declining numbers of specific CD4 T cells, but persistent humoral memory after certain vaccinations such as against yellow fever. The authors further speculate that these pre-existing virus-specific T cells against hCoVs might be one of the reasons why children and younger patients, usually considered to have a higher incidence of hCoV infections per year, are seemingly better protected against SARS-CoV-2. Unlike specific CD4 T cells found in RHDs, most S-specific CD4 T cells in COVID-19 patients displayed a phenotype of recent in vivo activation with co-expression of HLA-DR and CD38, as well as variable expression of Ki-67. In addition, a substantial fraction of peripherally found HLA-DR+/CD38+ bulk CD4 T cells was found to be refractory to peptide stimulation, potentially indicating cellular exhaustion.

Limitations

This is one of the first preprints reporting the detection of virus-specific CD4 T cells in COVID-19 (also cf. Dong et al., https://www.medrxiv.org/con... Weiskopf et al., https://www.medrxiv.org/con... "https://www.medrxiv.org/content/10.1101/2020.04.11.20062349v1.article-info)"). While it generally adds to our current knowledge about the potential role of T cells in response to SARS-CoV-2, a few limitations, some of which are discussed by the authors themselves, should be addressed. Findings in this study pertain to a relatively small cohort of patients of variable clinical disease. To corroborate the observations made here, larger studies including both more healthy donors and more patients of all clinical stages are needed to better assess the function of virus-specific CD4 T cells in COVID-19. Specifically, the presence of pre-existing, potentially hCoV-cross-reactive CD4 T cells in healthy donors needs to be explored in the context of COVID-19 immunopathogenesis. While the authors suggest a potentially protective role based on higher incidence of hCoV infection in children and younger patients, and therefore a presumably larger pool of pre-existing virus-specific memory T cells, the opposite could also be the case given cumulatively increased number of hCoV infections in older patients. In this context, it would therefore have been interesting to also measure anti-hCoV antibodies in COVID-19 patients. Furthermore, this study did not quantify virus-specific CD8 T cells. Based on observations in SARS-CoV-1, virus-specific memory CD8 T cells are more likely to persist long-term and confer protection than CD4 T cells, which were detected only at lower frequencies six years post recovery from SARS-CoV-1 (cf. Li CK et al., Journal of immunology 181, 5490-5500.) Morover, no other specifities such as against the N or M epitopes were evaluated. Robust generation of virus-specific T cells against the N protein was shown to be induced by SARS-CoV-2 in another pre-print by Dong et al. (Dong et al., https://www.medrxiv.org/con... "https://www.medrxiv.org/content/10.1101/2020.03.17.20036640v1)"), while Weiskopf et al. recently reported preference of both CD8 and CD4 T cells for S epitopes https://www.medrxiv.org/con... "https://www.medrxiv.org/content/10.1101/2020.04.11.20062349v1.article-info)"). Moreover, the authors seem to suggest that some of the virus-specific CD4 T cells detected could be potentially cross-reactive to predicted SARS-CoV-1 epitopes present in the peptide pools used. Indeed, this has been recently established for several SARS-CoV-2 binding antibodies, while it was found not to be the case for RBD-targeting neutralizing antibodies (cf. Wu et al., https://www.medrxiv.org/con... Ju et al., https://www.biorxiv.org/con... "https://www.biorxiv.org/content/10.1101/2020.03.21.990770v2)"). A similar observation has not been made for T cells so far and should be evaluated. Finally, since reactive healthy donors were only tested for anti-S1 IgG, however not for other more ubiquitous binding antibodies, e.g. against M, and only a fraction of these donors was additionally confirmed to be negative by PCR, there is, though unlikely, the possibility that some of the seronegative reactive donors had been previously exposed to SARS-CoV-2.

Significance

Quantification of virus-specific T cells in peripheral blood is a useful tool to determine the cellular immune response to SARS-CoV-2 both in acute disease and even more so post recovery. Ideally, once immunogenic T cell epitopes are better characterized, tetramer assays will allow for faster and more efficient detection of their frequencies. Moreover, assessing the potential role of pre-existing virus-specific CD4 T cells in healthy donors in the context of COVID-19 pathogenesis will be of particular importance. The observations made here are also highly relevant for the design and development of potential vaccines and should therefore be further explored in ongoing research on potential coronavirus therapies and prevention strategies.

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

On 2020-05-27 17:48:21, user John G. wrote:

I'm a non health or research person. But I thank you and others who are quickly researching and reporting on observations. We don't know exactly how it interacts but these results could be very promising. Thank you for sharing this.

On 2021-01-12 17:11:09, user sultan mehmood kamran wrote:

https://doi.org/10.1371/jou...<br /> article is published in PLOS ONE

On 2022-02-01 21:24:21, user Dylan wrote:

Would have been nice to see loss of taste and smell included given their pediatric prevalence per https://link.springer.com/a...

On 2020-09-20 04:37:16, user nkeegel wrote:

I don't have any numbers, but my impression is that the season in Australia did not influence onset or severity.

On 2020-12-16 21:08:32, user Dieudonné Balike wrote:

This is a preprint, not yet accepted for publication

doi: https://doi.org/10.1101/202...

On 2020-02-13 21:52:14, user reuns wrote:

I deduce from "case 13: no viral RNAs were detected until the fourth upper respiratory samples" that in the graphic U means negative

On 2020-09-29 22:53:36, user Guillermo Ruiz-Irastorza wrote:

The paper has been already published in PLoS One 2020 Sep 22;15(9):e0239401. doi: 10.1371/journal.pone.0239401. eCollection 2020.

On 2020-07-21 16:01:20, user OxImmuno Literature Initiative wrote:

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

On 2020-07-21 13:22:43, user Evolution 321 wrote:

Preprint implies an intention to formerly publish at a later time. Where has this manuscript been submitted for peer review? What journal was this intended for?

On 2021-02-02 16:30:41, user Martha Albertson wrote:

This is a poorly-designed study that looked at very few trials of ivermectin. The authors picked the studies that portrayed ivermectin in the worst light and ignored the many studies showing that ivermectin is a safe and effective treatment for Covid-19. I wonder who funded this study. Ivermectin is so much more effective than the expensive treatments promoted by the pharmaceutical industry. I can't imagine this biased study will survive peer review.

On 2020-12-05 01:38:02, user ACE NYPD wrote:

I have been using Betadine Gargle (.05% Povidine Iodine) as a gargle & nasal spray for months at 3 or 4 times a day. My wife, who has comorbidities also uses it. I have been exposed to Covid at least 4 times by others at work, and have always come back negative. Since I am in Tech Support, I have used keyboards and mice of infected persons. I am currently working from home until my latest exposure is 14 days since exposure. I took a rapid test that came back negative 6 days after the exposure, but I am still waiting on the PCR test I took the same day.

I also take a vitamin D supplement.

Do I think that the Betadine Gargle is preventing me from getting Covid, yes I do, but of course talk to your physician first. I have found these articles about Povidine Iodine and Covid:

https://www.pulmonologyadvi...

https://doi.org/10.1177/014...

https://www.thailandmedical...

Stay safe and informed.

On 2022-08-29 13:47:58, user Titos wrote:

This was published in NEJM as https://www.nejm.org/doi/fu...