1. Last 7 days
    1. On 2020-08-12 09:54:15, user kdrl nakle wrote:

      The whole paper is only presenting data and makes no estimates. "There is evidence of a considerable excess of deaths". Really?

    1. On 2023-12-28 09:01:29, user Till Dembek wrote:

      Dear colleagues,<br /> I congratulate you for conducting a well-planned study for investing the relationship between tremor and DRTT activation - and for allowing discussion of your<br /> results by publishing a preprint. However, I strongly discourage you from overinterpreting your “slope=1” relationship as prove of DRTT activation being causal for tremor suppression.

      This absolute value of the slope is, in my opinion, meaningless and purely coincidental. For this to be a true finding with absolute meaning, all your underlying steps would also need to be true. Your lead localization would need to be true, the way you track and threshold the DRTT would need to be true, the way you identify tremor from accelerometry would need to be true, and most importantly, the way you measure “stimulation spread” and relate this to DRTT activation would need to be true – none of which is probably the case.

      That there was a strong relationship between tremor suppression and DRTT overlap once again highlights the possible importance of the DRTT. I would find the results of this well conducted study far more convincing, if all the exclusion of datapoints, smoothing, normalization, relativization etc. were to be removed and “raw” correlations/regressions with their respective goodness of fit parameters were to be shown – no matter the absolute “slope” of these results.

      One additional point:<br /> While you apparently included several random effects in your analysis, which are not reported upon, you do not address stimulation spread / stimulation amplitude as the main confounding factor. Stimulation amplitude alone will<br /> explain a lot of the variance in tremor improvement – and is of course highly correlated to DRTT activation, so that it is difficult to disentangle the two.

      Best regards from Cologne!<br /> ~Till Dembek

    1. On 2022-08-06 10:16:33, user Jef Baelen wrote:

      No inclusion/exclusion criteria are mentioned? It includes a study from 2004, long before SARS-CoV-2 emerged. The Caruhel study was not performed on COVID-19 patients. The çelebi study used a cycle treshold cut-off of 38 and evaluated 20 parameters of which masks was only 1. The results of this study were wrongly extrapolated in table 1. Very dubious studies included in this meta-analysis!

    1. On 2021-10-05 09:40:08, user leecanning123 wrote:

      A major issue is that the pcr test is being used in this study, it is well known pcr produces false positives and as such any one of the placebo cases could be illness that is not connected to sarscov2, much like millions of "cases" around the world over the last 20 months. The FDAs own document stated that early pcr was based on "contrived" samples, meaning, not even real sarscov2.

    2. On 2021-08-01 16:03:29, user T Drive wrote:

      The CFR for SARS-CoV-2 is below that of average seasonal flu. Forced vaccinations using a product under an EUA is not warranted. If you want it, fine. Don't side with tyranny and try to force others to comply with your fearful beliefs.<br /> Per Table S-4, in trial recipients 15 with the vax died vs 14 with placebo.

    3. On 2021-08-01 21:15:17, user BiotechObserver wrote:

      You seem to be equating severe adverse reactions with severe covid, when these are not the same thing and not the same degree of danger. They reported there were 0 grade 4 reactions, for example. As for severe reactions in the placebo group are you expecting there to be severe reactions from a saline placebo injection? People getting fever, lethargy, chills, etc from the vaccine shot is not a counterpoint against the shot's efficacy against severe covid. Your arguments are not formulated well.

      "I’m assuming that reducing PCR positivity if you have a mild illness isn’t what most people are really interesting."

      The VE estimates are not reflecting "reducing PCR positivity" - Did you read the study? The VE is measured on symptomatic cases. Asymptomatic cases were not tracked. And severe covid cases were reduced dramatically, as you mentioned yourself.

    1. On 2020-09-01 09:40:12, user Roland Salmon wrote:

      This is a thorough piece of field epidemiology, although like much field epidemiology today, the data substantially comes from existing information sources. As a former director of the Communicable Disease Surveillance Centre Wales (CDSC), I am pleased that Public Health Wales, via CDSC staff, past and present, produces work of this quality.

      The study demonstrates, persuasively, that much of the problem with infection in care homes, resulted from the care home's size, rather than from receiving infected patients, discharged from hospital. Nevertheless, I do not think that it should be stated ("Research in context"p.3) that "Our analysis found no effect of hospital discharges on care home outbreaks once care home size had been adjusted for" (my underline). In fact, as the discussion section makes clearer (p11), the observed hazard ratio is 1.15 and the effect could be as high as 1,47 (Table 2), although the result is not statistically significant at the 5% level. (It would be interesting inter alia to know the actual probability of this, the most probable estimate of hazard of 1.15.) Table 3, looking at the risk of outbreaks, by care home capacity, further, implies that the effect of discharges might be particularly marked in the smaller homes (<10 beds) where I calculate that the crude relative risk of an outbreak in the post hospital discharge risk period is 3.2. compared with around 1.2 for larger homes. Anyway, an intervention that reduced the risk of outbreaks, in this vulnerable population, by some 15% would be considered by most people as well worth having.

      It's thus important to reflect whether the failure to demonstrate an effect of this size merely reflects a lack of statistical power, some of which could be due to misclassification of the outcome. The study authors recommend, in "Conclusions and recommendations" (p12), that, "further analyses should investigate the risk where discharges were confirmed or probable cases of Covid-19, and also consider additional evidence on likely chains of transmission that may become available from sources such as.....viral genetic sequence data". This is an important supplementary piece of work. In addition, the risk from hospital discharges, unlike that from home size, does not extend over the whole period of the study. I note that 16 outbreaks that occurred before certain homes received any discharges are included in the dataset so homes, therefore, enter the study before they are at risk of any infection introduced by receiving patients discharged from hospital. Secondly, homes remain in the study after 2nd May, when universal testing of hospital patients for SARS CoV2, prior to discharge to care homes, is introduced. Thus, from, a few days after this until the 27th June, the study's end date, effectively, risk from hospital discharges is eliminated whereas the risk from home-size remains. The authors consider this and report that they fitted their model, with a factor for the two time periods (before and after 2nd May). They tell us that, "this factor was found not to be significant, and did not significantly alter the hazard ratios". Whilst I understand that any alteration of the hazard ratios was not significant at alpha =5%, I would like to actually see the change in the observed hazard ratios. It might be expected that the hazard of receiving hospital discharges was higher in the period up to 2nd May, than in the period from 2nd May to the study's end.

      I was curious as to why Cox's Proportional Hazard was the test used. I don't altogether see that the risk of outbreaks following introduction, by hospital discharge is particularly time dependent, given how readily and for how long SARS CoV 2 can spread in institutional settings. Thus, I don't really see why that risk factor could not be expressed as a categorical variable (outbreak, no-outbreak) which would allow a much simpler analytical approach. I, frankly, also, don't understand the detail of the sensitivity analyses, presented, for choosing different at-risk time periods which, I feel, for a general readership, certainly, merits being explained more fully.

      Finally, I think that the discussion section could be more robust. If home size is the issue, then shouldn't the authors be saying that larger homes need to consider having dedicated areas, facilities and staff for smaller subsets of their residents. Maybe larger homes should have more stringent planning requirements. I also think that rather more should be made of the contribution of hospital discharge (notwithstanding it's failure to achieve conventional 5% levels of statistical significance) than the rather anodyne paragraph at the foot of page 11 which bears all the hallmarks of the dead hand of the corporate public relations department.

      Nonetheless, overall, this is an accomplished piece of epidemiology with important practical implications.

      Dr Roland Salmon

    1. On 2020-06-08 21:08:42, user Paul Gordon wrote:

      Hi, nice work. I notice that NRW-11 is reported in the supplementary tables, but is the only genome missing in GISAID. Was it withdrawn due to quality or was there an oversight in the submission? Thanks!

    1. On 2020-06-15 21:36:07, user Marm Kilpatrick wrote:

      Fantastic (but worrisome) work! <br /> Would it be possible to give the full details of the regression of infectious viral load via culturing (PFU/ml) vs RNA via qPCR? This relationship is robust and could be used as the basis for inferring infectious viral load from qPCR, but doing so in a way that explicitly incorporates uncertainty would require more details of the regression than you currently report. Specifically, if you could report the slope, intercept and residual standard error and sample size for this regression that would enable others to make maximal use of your results. Even better would be to make the individual data points from graph available and then the data could be used directly.<br /> Thank you very much for this important work!<br /> marm

    1. On 2020-09-06 08:30:14, user Aporia wrote:

      No matter how you criticize the data- every argument still places these estimates FAR lower then what the media has been pushing . Add to that Dr Ioanidis's talks - we did this by being pushed into a panic- the total years of life lost this season due to Covid is on par wt a flu, but the lockdown will cause REAL LIVES LOST - via deaths of despair (suicides, crime, od etc)

    1. On 2021-06-15 18:52:28, user Quixander wrote:

      That’s not necessarily the case re real vs contrived. The immune system may be “keyed” to only the real and original virus, and may not recognize significant variants the more different from the original they become. The neat thing about mRNA vaccine is that a specific protein was strategically chosen as the “key” that, based on many years of research and analysis, was believed to be most likely preserved across many future mutations. In this way, the mRNA vaccine is very likely to provide better immunity to a changing virus.

    1. On 2021-09-08 09:10:08, user Kenneth Coville wrote:

      Actually your quote contradicts your claim.

      'There are now several studies" (claim)

      “To my knowledge, it’s the first time [this] has really been shown" (quote)

    2. On 2021-09-10 13:28:05, user Ben Veal wrote:

      The hospitalization rates are not in favour of vaccination (the study shows 8 times more hospitalizations in the vaccinated group compared with the pre-infected group). Even after my worst case scenario correction (which assumes some unaccounted for cofactors caused all the deaths) the difference in hospitalizations is not significant.

    3. On 2021-08-26 11:54:58, user Gubbedefekt wrote:

      Can someone confirm: what difference did it make if the natural immunity was acquired from a delta variant infection compared with one from another variant? Did the study look at this?

      In any case the comparison looks devastating for Pfizer and other vaccine producers.

    4. On 2021-09-07 02:07:49, user jagmarz wrote:

      You're completely missing the point that in order to get to post-infection immunity, you have to get infected first. Meaning you have had the opportunity to participate in the spread, and the fact that NOW you're less likely to spread Covid-19 is really nice but how does that make up for the spreading you may have done while actually infected?

    5. On 2021-10-05 14:28:59, user Costel Atanasiu wrote:

      "If you think humoral immunity is superior to or equal to cellular immunity, then you flunked Immunology 101"

      Explain!

    6. On 2021-09-03 04:14:55, user Hucello Chuyucello, PhD wrote:

      It looks like it is both multivariate and multivariable modelling, however I do not see any accounting for multiple testing.

    7. On 2021-09-09 17:46:01, user bgoo2 wrote:

      That is patently false. And there is no credible information ANYWHERE that it is dangerous to receive a Covid vaccine months after you've recovered from covid.

      Immunity from past infection is dramatically increased by ALSO getting vaccinated.

      This is demonstrated very clearly in multiple peer reviewed studies. And I'm not doing the work here to look start citing study links to people who can't be convinced by MATH.

      Self-proclaiming you are "pro-science" doesn't make you pro science. No, natural immunity is NOT superior. And the numbers in every single hospital everywhere in the world clearly show that.

      If natural immunity to these strains was superior... the WORLD would not see 80-90% of it's CURRENT hospitalizations from unvaccinated and partially vaccinated. The fact that the 80-90% number does not resonate with you... or anyone else with neurological conditions here... makes it a waste of time for me to be typing this.

      So I have no one to blame for this reply but myself I guess.

    8. On 2021-08-29 21:38:00, user MANISH JOSHI wrote:

      We must stop ignoring natural immunity - it’s now long overdue<br /> Manish Joshi, MD

      This article by Gazit et al is another addition to a growing body of literature supporting the conclusion that natural immunity confers robust, durable, and high-level protection against COVID-19 (1-4). Yet some scientific journals, media outlets, and public policy messaging continue to cast doubt. That doubt has real-world consequences, particulary for resource limited countries. We would like to review available data.

      Infection generates immunity. The “SIREN” study in the Lancet addressed the relationships between seropositivity in people with previous COVID-19 infection and subsequent risk of severe acute respiratory syndrome due to SARS-CoV-2 infection over the subsequent 7-12 months (1). Prior infection decreased risk of symptomatic re-infection by 93%. A large cohort study published in JAMA Internal Medicine looked at 3.2 million US patients and showed that the risk of infection was significantly lower (0.3%) in seropositive patients v/s those who are seronegative (3%) (2).

      Perhaps even more important to the question of duration of immunity is a recent study that has demonstrated the presence of long-lived memory immune cells in those who have recovered from COVID-19 (3). This implies a prolonged (perhaps years) capacity to respond to new infection with new antibodies.

      In contrast to this collective data demonstrating both adequate and long-lasting protection in those who have recovered from COVID-19, the duration of vaccine-induced immunity is not fully known- but breakthrough infections in Israel, Iceland and in the US suggests few months. Before CDC decided to stop collecting data on all breakthrough infections at the end of April, 2021, it reported >10,000 breakthrough infections (2 weeks after completion of vaccination) in the US, with a mortality of ~2% (5). Booster COVID vaccine recommendations have been already announced in Israel and in the US proving ineffectiveness within 6 months.

      How should we use the collective data to prioritize vaccination? These new data support simple and logical concepts. The goal of vaccination is to generate memory cells that can recognize SARS-CoV-2 and rapidly generate neutralizing antibodies that either prevent or mitigate both infection and transmission. Those who have survived COVID-19 must almost by definition have mounted an effective immune response; it is not surprising that the evolving literature shows that prior infection decreases vulnerability. In our view, the data suggest that people confirmed to have been infected with SARS-CoV-2 may not need vaccination. We should not be debating the implications of prior infection; we should be debating how to confirm prior infection (6).

      Manish Joshi, MD<br /> Thaddeus Bartter, MD<br /> Anita Joshi, BDS, MPH

      1. Hall VJ, Foulkes S, Charlett A et al. SARS-CoV-2 infection rates of antibody-positive compared with antibody-negative health-care workers in England: large, multicentre, prospective cohort study (SIREN). Lancet. 2021
      2. Harvey RA, Rassen JA, Kabelac CA, et al. Association of SARS-CoV-2 Seropositive Antibody Test With Risk of Future Infection. JAMA Intern Med.
      3. Turner, J.S., Kim, W., Kalaidina, E. et al. SARS-CoV-2 infection induces long-lived bone marrow plasma cells in humans. Nature 2021
      4. Wang, Z., Yang, X., Zhong, J. et al. Exposure to SARS-CoV-2 generates T-cell memory in the absence of a detectable viral infection. Nat Commun 12, 1724 (2021).
      5. https://www.cdc.gov/mmwr/vo...
      6. Kuehn BM. High-Income Countries Have Secured the Bulk of COVID-19 Vaccines. JAMA. 2021;325(7):612
    9. On 2021-10-07 17:57:06, user 4qmmt wrote:

      It simply means that there was not enough data to conclude, within the selected confidence interval (95% in this case) that the reduction was not due to chance.

      But if there was not enough data to conclude, why did they make that conclusion?

    1. On 2021-08-10 16:31:12, user Jeff Brender wrote:

      "The 95% confidence interval (CI) of the IRR was calculated using an exact method described previously.(ref.12)"<br /> ref 12 Sahai H, Khurshid A. Statistics in Epidemiology: Methods, Techniques and Applications. CRC Press; 1995

      The exact method should probably be specified here

    1. On 2020-04-24 09:51:12, user Rajendra Kings Rayudoo wrote:

      TO<br /> Kamalini Lokuge, Emily Banks, Stephanie Davis, Leslee Roberts, Tatum Street, Declan O'Donovan, Grazia Caleo, Kathryn Glass

      I rea the above paper very happy to listen the decline of carona in Australia but as you mentioned the measures to take in the populous country likeindia which is 70 times bigger than Australia but the mathematical models and the way of finding asymptomatic carriers are fascinating

      i request you to please explain the methods of conducting the efficient way to eradicate the asymptomatic carriers

      thanking you <br /> with regards <br /> rajendra

    1. On 2021-01-31 22:01:02, user Pablo Olavegogeascoechea wrote:

      I have read this trial with great interest and I have some worries about some detalles: fist of all, the absolute risk reduction is quite low (1.4%) and the NNT for the primary outcome is 70 as it is for hospitalization. On the other hand there were more patient who developed pulmonary embolism in the Colchicine group (may be this issue needs more infromation)

    1. On 2021-08-10 14:49:04, user Dr. Chris Bird wrote:

      This looks like very nice work. You have not, however, estimated "Total Immunity" as claimed. You have estimated how many people have been infected, which is very useful. To get "total immunity", you have to incorporate the growing body of literature on the probability of not being immune even if you have recovered (Cavanaugh et al 2021) or been vaccinated (Sheikh et al 2021 as one example). That will substantially decrease the estimate of immune and help to explain why the July-August 2021 surge is occurring.

    1. On 2022-05-03 19:26:37, user Carol Taccetta, MD, FCAP wrote:

      The MMIA assay used here comes from the same institution as the authors--the reference states it is under a provisional patent.

    1. On 2019-10-16 12:50:12, user GuyguyKabundi Tshima wrote:

      EVOLUTION OF THE EPIDEMIC IN THE PROVINCES OF NORTH KIVU AND ITURI AS AT OCTOBER 12, 2019<br /> Sunday, October 13, 2019<br /> Since the beginning of the epidemic, the cumulative number of cases is 3,218, of which 3,104 confirmed and 114 probable. In total, there were 2,150 deaths (2036 confirmed and 114 probable) and 1032 people healed.<br /> 429 suspected cases under investigation;<br /> 6 new confirmed cases to CTEs, including;<br /> 4 in North Kivu, including 2 in Beni and 2 in Kalunguta<br /> 2 in Ituri, including 1 in Mandima and 1 in Nyakunde;<br /> 2 new confirmed deaths, including:<br /> 1 community death in North Kivu in Kalunguta;<br /> 1 new confirmed death in CTE in North Kivu in Beni;<br /> 1 person healed out of CTE in Ituri in Mambasa;<br /> No health workers are among the newly confirmed cases. The cumulative number of confirmed / probable cases among health workers is 161 (5% of all confirmed / probable cases), including 41 deaths.

      NEWS

      New health area infected with Ebola virus in Ituri<br /> - A new Health Area has been affected by Ebola Virus Disease in Ituri. This is the Maroro Health Area in the Nyakunde Health Zone;<br /> - Indeed, Nyakunde was already at 294 days without notifying a new confirmed case of the EVD and returned to zero following this new affection;<br /> - Of all the 6 cases reported this Sunday, October 13, 2019, none of them were listed as contact, nor monitored regularly or vaccinated;<br /> - It is also reported that the alerts of all these cases are coming back from the community and their contacts are being listed, the investigations are continuing, the decontamination of the patients' households is being carried out and the ring of vaccination has been opened around all these cases.

      VACCINATION

      • Since the beginning of vaccination on August 8, 2018, 237,632 people have been vaccinated;
      • 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 105,518,454 ;
      • 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.
    1. On 2020-12-27 02:14:14, user valley_nomad wrote:

      What is the definition of mortality rate in this study? The numbers seem to be way too high if it is CFR (case fatality rate).

    1. On 2020-06-01 14:11:35, user Anne Thomas wrote:

      It's a shame there was no differentiation between UVA and UVB. UVB is blocked by the atmosphere so is more abundant at higher altitudes and of course it's UVB which is responsible for vitamin D synthesis, supporting the vitamin D hypotheses, which is of course supported by 7 preprints. https://www.bmj.com/content... and what we were predicting based on the known role of vitamin D in immunity and reducing inflammation. It appears that vitamin D is particularly important in Covid-19 in preventing a cytokine storm.

    1. On 2023-10-09 09:09:13, user Susie Huntington wrote:

      The article has now been accepted for publication by the European Journal of Cancer Prevention without edits and will be published shortly.

    1. On 2021-08-11 01:11:43, user dustinst22 wrote:

      you are forgetting that vaccination lowers CFR. The more of a population with seroprevalence, the lower the mortality rate. This doesn't mean delta is less virulent, it means there is more population protection.

    1. On 2025-08-26 09:32:57, user Constant VINATIER wrote:

      Feedbacks about your preprint : https://doi.org/10.1101/2025.08.08.25333030

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

    1. On 2020-03-31 20:27:36, user Andrew Singer wrote:

      Can the authors please check the validity of the first reference that is cited. It does not report SARS-CoV-2 in stool. It is a paper on: "Elagolix for Heavy Menstrual Bleeding in Women with Uterine Fibroids"

      A second comment is that you state: 17 patients (23.29%) remained positive in feces after viral RNA was undetectable in respiratory tract, however, there were only 39 patients that initially tested positive for viral RNA in the stool, so it should be 17/39 (43.58%). Yes?

    1. On 2020-04-19 18:41:29, user Dean Karlen wrote:

      The authors are reporting incorrect confidence intervals because they to not correctly treat the unknown false positive rate. Use the manufacturer data for false positives (2 out of 371 known negatives) to give the posterior probability for the false positive rate (fpr) which is proportional to Binomial(2, 371, fpr). With this, calculate the 95% CL interval using the exact approach (Neyman). The correct interval, for the unadjusted case is:

      [0.00% - 1.53%]

      The authors report an incorrect interval for this case: [1.11% - 1.97%].

      Because the unadjusted case is such a simple problem to interpret, there is only one correct treatment to produce the 95% central confidence interval. Done correctly, and reporting the correct intervals, this paper would not gain any attention at all. Please ignore this paper. It is only getting attention because the authors made serious mistakes in the analysis. The authors should retract this erroneous paper.

      Python code with this calculation will be provided to anyone on request. I have contacted the lead author, pointing out their error in statistical analysis. I have received no response.

    2. On 2020-04-25 20:51:41, user outdoorgirl0814 wrote:

      Given that the death counts are generous, it seems unlikely that we are underestimating the death count. Anyone who dies and had symptoms similar to COVID is now counted as a COVID-19 death, and anyone testing positive who dies, regardless of whether it was from COVID, is also counted as a COVID death. This is probably inflating the numbers of COVID deaths we are seeing, but it seems the public health officials believe it to be better to err on the side of inflated numbers, so as avoid underestimating he lethality of the virus. So, if a greater percentage of people test positive than we originally thought, we have been inflating the numerator and underestimating the denominator and that would mean we are grossly overestimating the case fatality rate. That is, unless there are a large number of bodies somewhere that aren't being included in any of the mortality counts. It seems like it would be unlikely for a significant number of people to be dying of unknown causes during this pandemic, with no other symptoms and who constitute untested COVID-19 positive patients, with no one noting it.

    1. On 2020-10-21 23:20:22, user Melimelo wrote:

      Very useful study. Any chance you could do this study with warm salt water as one of the gargling solutions? maybe try different salt concentrations?

    1. On 2021-04-23 07:42:37, user The Crane Report wrote:

      "The authors have declared no competing interests"<br /> Sinetra Gupta received almost £90,000 from the Georg and Emily von Opel Foundation to fund research “into the prevalence of COVID-19 in the population” in the first week of April 2020.<br /> https://www.opendemocracy.n...

    1. On 2020-08-14 22:32:38, user Andrew Foers wrote:

      Really nice work, and a great resource! Looking forward to your future reports.

      If I was reviewing this I'd ask for more information about the control subjects. Without details as to how the control subjects were processed, we are unable to judge if preparation differences in the control cohort contirbute to sample classification.

    1. On 2020-02-28 02:55:16, user Art Enquirer wrote:

      Will it be possible for an AI startup (actually a hackathon team) to secure access to your data? Will you share for the sake of the world? We are also running servers with AI algorithms and wish to pre-test your conclusion.

    1. On 2020-07-15 17:27:42, user Nicholas DeVito wrote:

      The authors identify this trial as NCT04438629.

      This registry entry is available here: https://clinicaltrials.gov/...

      This entry does not mention treatment with Baricitinib at all. Can the authors please update their clinical trial registry entry to accurately reflect the treatments under consideration in this study?

    1. On 2020-05-06 23:30:49, user Bárbara Souto wrote:

      Patients of the non-chloroquine group started to be monitored six days before the chloroquine group. Consequently, it is clear that the chloroquine group participants would have an early clearance of virus RNA. The median of day difference between start of symptoms and start treatment (monitoring) was 6 days. Exactly the same difference between the medians of viral RNA clearance day between the groups, as show in the KM curve. In fact, the results from this study strongly suggest that there is no effect of chloroquine on viral clearance.

    1. On 2020-05-08 17:47:49, user Markus Cornberg wrote:

      Dear Leif,<br /> very important data.<br /> we are also looking at this in Hannover (CD8 though). Maybe we can talk about this if you like<br /> Please look at these studies in mouse models to understand cross-reactive T cell responses.

      Anti-IFN-? and peptide-tolerization therapies inhibit acute lung injury induced by cross-reactive influenza A-specific memory T cells. Wlodarczyk MF, Kraft AR, Chen HD, Kenney LL, Selin LK. J Immunol. 2013 Mar 15;190(6):2736-46. doi: 10.4049/jimmunol.1201936. Epub 2013 Feb 13.

      All the best<br /> Markus

    1. On 2020-09-06 08:17:57, user Marc Girardot wrote:

      Agree with Helene Banoun<br /> Given the importance of cellular immunity in the case of a virus, this study does not prove its conclusion. "..., this study cannot conclude that there is no cross-immunity with HcoVs since it only measures humoral immunity (and for some antibodies only).".

      Effective Resident Effector Memory T-cells from other HcoVs have been proven to exist, and in the case of Covid-19, vaccine induced reaction produced. In larger number than regular traditional Memory Effector T-cells in the blood, with a large peptidic repertoire (70% genes in common with other HcoVs), it is quite probable and scientifically logical that they provide a powerful sentinel immunological protection directly in the tissue, even before the virus reaches the blood stream.

      Tissue-resident memory CD8 T-cell responses elicited by a single injection of a multi-target COVID-19 vaccine https://www.biorxiv.org/con...

    1. On 2020-10-07 06:13:12, user Markku Peltonen wrote:

      There were a number of comments on this manuscript on twitter early August, with concerns on errors in the calculations among others. Might be useful for others, so here is what I tweeted on August 5th 2020 (https://twitter.com/MarkkuP...: "https://twitter.com/MarkkuPeltonen/status/1290754970292281349):")

      Recently there was a meta-analysis on the effects of masks conducted in Finland. A number of comments has been made about the quality of the piece, so I had a quick look at it. As the analysis was also mentioned at least in Sweden, few quick comments in English. 1/10

      Background: the Finnish Ministry of Social Affairs and Health did a systematic review in May 2020 on the use of community face coverings to prevent the spread of Covid-19. There was no meta-analysis in the review, which focused on effectiveness. 2/10

      The conclusion on that report was “very little research data available on the effectiveness of community face coverings in preventing the spread of COVID-19 in society.” and evidence “minor” or “non-existent”. 3/10

      So, now then a formal meta-analysis, identifying the same 5 randomised controlled trials, showing an effect with relative risk estimate 0.61 (95% CI 0.39-0.96).<br /> Few points: 4/10

      The meta-analysis focuses on efficacy; what is achievable potentially when perfect conditions. They do something which they call “account of bias caused by non-compliance”; ie. if persons in the mask-group did not were masks they “adjust” for this. 5/10

      To me, this sounds quite controversial: In my world we look at intention-to-treat first, and then perhaps maybe on the “per-protocol”/“as treated”. <br /> Efficacy important, but this is now something different than what the original systematic review aimed at. 6/10

      The problems of this accentuate in the Discussion, where the authors do not seem to understand the difference in efficacy and effectiveness, nor the fact that they are actually analysing something else than the original review, and making way too far-fetched conclusions. 7/10

      There are other peculiarities, for example “Four of the analyzed studies evaluated the use of masks on respiratory infections directly, and in one the primary outcome was compliance with mask use.”. Hopefully an error, I don’t believe they actually mix the outcomes like this. 8/

      . @jejkarppinen added the following comments after my initial post, which I agree with:<br /> - The potential biases in the original papers were not covered.<br /> - Quality of evidence was not evaluated at all.<br /> - Dissemination of the results did not consider the potential problems. 9/10

      Finally:<br /> - I've not read the original 5 studies. <br /> - I’m not an expert on systematic reviews/meta-analyses. <br /> - I do think recommendation for masks is motivated, and the evidence is there (but not here..).<br /> - I do think we should be objective when evaluating evidence. 10/10

      The original systematic review the Finnish Ministry of Social Affairs and Health in Finnish is here (english abstract only):<br /> http://julkaisut.valtioneuv...

      Ps. Somebody noted the lack of preregistered protocol, which reminded me that the PRISMA-guidelines helpful when reporting systematic reviews and meta-analyses. <br /> Their checklist should be followed in reporting:<br /> http://prisma-statement.org

      In addition, it was noted by Jesper Kivelä that there are errors in the calculations, these should be corrected (in Finnish):<br /> https://twitter.com/JesperK...

    1. On 2021-09-09 18:08:45, user Jason Howard wrote:

      Overall, I applaud the authors for writing this manuscript. It's valuable data for public consumption. That said, I think the report would be more impactful if they also recorded which vaccine the vaccinated subjects had.<br /> It would be great if the authors mentioned what internal control gene (ex human RNAse P) the testing center (Exact Sciences Corporation,) used. I also think the authors should remind the readers that a lower Ct value corresponds to a higher viral titer.<br /> One item to mention is that some medical personnel do a better job of collecting a nose swab sample. The quality of collection can affect the Ct value. The authors should also consider citing the source of the estimated delta variant prevalence mentioned in the abstract.

    1. On 2020-05-30 18:48:21, user Craig Travis wrote:

      The endocannabinoid system plays a fundamental role in the immune system to reduce and resolve inflammation. A recent preprint showed that CBD reduced the expression of ACE2 and TMPRSS2, both of which are required by CoV2 to enter cells. The authors also stated that cannabis did the same. More research needs to be done to determine the risk or benefit of this class of drugs especially now during this pandemic without a prohibition-minded bias clouding the picture. Research has established the antioxidant properties of the inhaled substances. Not true for tobacco.

    1. On 2020-07-25 15:35:31, user wbgrant wrote:

      Without information on the vitamin D dose and serum 25-hydroxyvitamin D concentrations of the participants, no concluusion can be made regarding vitamin D from this study. See<br /> Grant WB. Re: Preventing a covid-19 pandemic: Can vitamin D supplementation reduce the spread of COVID-19? Try first with health care workers and first responders. BMJ. April 1, 2020 https://www.bmj.com/content...

    1. On 2020-08-28 17:49:17, user Jean Sanders wrote:

      this is excellent information ; it is extremely well written with good data and also it is accessible to the average lay person like myself. I found it fascinating and sent it to school committee members in Massachusetts in the city where I live. Important considerations for September -- some are predicting a peak in Dec. and then another in Feb depending upon what date the kids are back in school and how many are in a classroom etc. a lot of variables and contributing factors -- flatten the curve

    1. On 2020-03-29 12:55:46, user Rosemary TATE wrote:

      I'm about to submit a review for this - my first attempt on medrxiv although (as a medical statistician) I have vast experience. However, all I really needed to do was look at their Cherries checklist. It is very incomplete and missing many details of how the study was carried out. These checklists are very important and shouldn't be added as an afterthought.

    1. On 2020-09-16 17:00:31, user sunmaster14 wrote:

      Yeah, but it's not true that mortality only occurs in >=65yo. Worldwide, ICU admission and mortality for >=65yo is on the order of 25%. Applying that to the 154 old patients given standard care and the 10 old patients given HCQ would mean that 56 of the ICU admissions/deaths occurred for <65yo in the standard care pool, which is 1.6%, and 7 of the ICU admissions/deaths occurred for <65yo in the HCQ pool, which is 0.4%. You can obviously play around with the probability of >=65yo suffering morbidity/mortality with standard care, and get different relative results for HCQ on the <65yo subgroup, but using something so high that it implies everybody in ICU was >=65yo is obviously wrong.

    1. On 2024-05-02 14:51:48, user Kathy Tullos wrote:

      TSW research is imperative to validating (or invalidating) the patient experience. As it stands, the patient experience is invalidated by the medical community based on no research: "to date there have been no systematic clinical or mechanistic studies to distinguish TSW from other eczematous disorders." To confidently tell patients something is all in their heads while doing no research to prove or disprove that stance is truly unethical. Patients numbering in the thousands have been reporting these adverse effects for the past 10 years - including a cluster of new symptoms never experienced prior to topical steroid treatment - and it is roundly dismissed. "Steroid phobia" is thought to be the culprit. The finger is pointed at the patient for underusing, overusing, or going off treatment. The only reason patients go off this treatment is because the symptoms have escalated so extremely during treatment, there is nothing left to do but see if the treatment was the problem. Of course there is an acute phase after cessation of withdrawal. But after a protracted withdrawal phase, there is improvement. We see this pattern time and again in the patient community. All anecdotal of course. There has been no intellectual curiosity from the scientific medical community to drill down and see if there is validity or an explanation. That is why this study, and future studies that it will spark, is so very important. Thank you for listening to reports and for trying to understand and fix the problem. We need to connect patients with doctors and we can not do this if patients' reports are not believed. Doctors only really listen to other doctors. Another reason we need more research like this.

    2. On 2024-05-03 15:04:37, user Tamy wrote:

      I am happy to see someone taking an interest in this horrific condition. My daughter has suffered for over 9 years and the mental toll, as well as, the physical toll it has taken on her overall well being has been life changing! Thank you for giving these sufferers some validation!

    1. On 2021-01-17 17:03:45, user kdrl nakle wrote:

      Extremely important result. Shows aerosolization of the virus when it can be cultured from less than 0.5 micron particles, these are definitely aerosol size.

    1. On 2021-03-17 10:27:00, user Olaf Storbeck wrote:

      I took the Vitamin D data from that paper but pulled the Covid-19 data myself due to severe data errors I found in the figures (very similar to the other commentors). I also corrected the Turkey Vitamin D data to that from a much better meta analysis ((Alpdemir, Medine & Alpdemir, Mehmet. (2019). Vitamin D deficiency status in Turkey: A meta-analysis. International Journal of Medical Laboratory. 10.14744/ijmb.2019.04127).<br /> The analysis in this preprint it fully dominated (beside the data errors) from the Czech data point, which is clearly an outlier and unfortuneatly not even shown in Figure 1.

      When correcting the failures I got a significant correlation of Vitamin D deficiency to Covid-19 cases and deaths with p values on 0.0005 to 0.02 range.

    1. On 2021-08-21 16:43:18, user Mark J Kropf wrote:

      A good many issues are of question in regards to this work, after mulling it over a good time. Firstly, evolution is always going on. If one is defining mutations in the most general sense, no treatment alters that rate. However, if one means by mutation the generation of some particularly problematic change causing a variant, then perhaps the logic dealt with here is relevant. Evolution is not a process which can be terminated or quelled, though it may be channeled and controlled! Secondly, a period of about 5.5 months can give some possible resonance to the supposed finding, but the ability to alter progression needs to really have significant follow up. Is the process of some unfavorable change (i.e my latter use of 'mutation' above) really limited or is it only impeded and delayed? A true ability to confirm requires a longer period of analysis and the current argument conclusion may be somewhat presumptuous in its statement. Thirdly, I am concerned that the numbers may yet be a bit too small for the conclusion reached, though running a study with the proper enrolled numbers for such comparisons is probably too problematic to be practical.

      I believe there is some evidence here, but perhaps not so complete as to be given the full impact that the conclusion provides. It is likely, but it is not confirmed to nearly the extent that I might desire for such a paper.

    1. On 2020-05-15 08:15:51, user Ron Sills wrote:

      Maybe they should look into the anti-h factor in the blood type or bombay and para-bombay influence on the infection rate and mortality rate. That might better explain the minor differences in percentage rates for the O blood group.

    1. On 2020-05-11 12:23:34, user Sinai Immunol Review Project wrote:

      The main finding of the article: <br /> This study analyzed the prevalence of vitamin D insufficiency (VDI) among SARS-CoV-2 positive subjects hospitalized in a medical center situated in New Orleans. Through medical records, the authors performed a retrospective review of 20 Covid-19 patients with serum 25-hydroxycholecalciferol (25ODH) levels determined. Vitamin D insufficiency (VDI) was defined as a serum 25OHD < 30 ng/mL. Among these patients, 65% required intensive care unit (ICU). When they analyzed the 25ODH levels, 84.6% of ICU subjects presented VDI in compare to 57.1% of floor subjects. Curiously, 100% of ICU patients less than 75 years old had VDI. In addition, the authors demonstrated that lymphocytopenia was present in 92.3% of the Covid-19 patients admitted to ICU. Among the clinical and demographic characteristics of SARS-Cov-19 ICU patients of this study we can highlight: 84% of the subjects were African American, hypertension and diabetes was presented in 76.9% and 46.2% ICU and non-ICU patients respectively, the body mass index of 100% of the patients was considered overweight or obesity, and all had high levels of lactate dehydrogenase.

      Critical analysis of the study: <br /> The manuscript data and patient description is well presented. However, the number of patients analyzed is very small to extract meaningful conclusions. The manuscript has a comprehensive discussion on the effects of VDI in prothrombosis and inflammation. The presence of vitamin D receptors in lung epithelial cells and macrophages suggests that the influences of vitamin D (VD) is relevant for respiratory health. It is known that active VD acts by reducing inflammation in human airway smooth muscle cells and influences airway barrier integrity. In addition to increasing the study population, the authors could have analyzed the direct correlation between VDI and lung damage (using specifics parameters like tomography and arterial blood gas analysis), since these exams are often prescribed to patients with severe acute respiratory syndrome.

      The importance and implications for the current epidemics: <br /> VDI is highly prevalent in dark-skinned individuals, and in the Italian and Spanish populations. VDI could thus contribute to Covid-19 severity disease in these populations, as VD plays an essential role in modulating the innate and adaptative immune response. This manuscript suggests that healthy levels of VD, through controlled supplementation, can help the immune system to protect against respiratory diseases like SARS-CoV-19.

      Reviewed by Bruna Gazzi de Lima Seolin.

    1. On 2021-10-03 18:28:32, user Joseph Psotka wrote:

      It would be much more useful to look ar discrepancies in the immune system of the twins. Even dizygotic twins can have the same immune system.

    1. On 2020-05-08 13:34:09, user Sinai Immunol Review Project wrote:

      Title: <br /> Homologous protein domains in SARS-CoV-2 and measles, mumps and rubella viruses:<br /> preliminary evidence that MMR vaccine might provide protection against COVID-19<br /> The main findings of the article: <br /> This work aimed to determine whether measles, mumps and rubella (MMR) vaccination might provide protection against COVID-19. The authors examined: 1) sequence homologies between SARS-CoV2 and measles, mumps and rubella viruses; 2) correlations between MMR vaccination coverage, rubella antibody titers, and COVID-19 case fatality in European countries. <br /> Sequences of measles, mumps and rubella virus, which are component of MMR vaccine, were aligned to SARS-CoV-2 to identify homologous domains at the amino acid level. The Macro domain of rubella virus p150, a protease) aligned with SARS-CoV-2 Macro domain of non-structural protein 3 (NSP3), also a protease, at 29 % amino acids identity, suggest similarity in protein folding. Residues conserved in both strains include surface-expressed residues and residues required for ADP-ribose binding, and ADP-ribose 1” phosphatase (ADRP) enzymatic activity. Although the Macro domains are within a cytoplasmic non-structural protein, the authors speculate that they could contribute to vaccine antigenicity if released upon cell lysis. Measles and mumps, both paramyxoviruses, showed structural homology between their F proteins and SARS-CoV-2 spike protein. Both F proteins and spike proteins are responsible for fusion of viral and cellular membrane. The sequence identity was 20 % over a 369-amino acid region and surface-exposed residues were well conserved.<br /> The examination of historic vaccination schedules or recommendations for MMR vaccination in Italy, Spain and Germany revealed that populations who are currently in the age group of 40-49 years old in Germany, 30-39 years old in Spain, and 20-29 years old in Italy were vaccinated. However, the rubella vaccine was introduced for pre-adolescent girls and campaigns for women in child bearing age were conducted early 1970s to 90s in each countries. The latter might cover the women who are currently in the age group of 59-69 years old. If MMR is indeed protected for COVID-19 fatality, the above analysis would suggest that older populations and males are both more likely to die from Covid-19, and less likely to be seropositive for rubella specific immunity. <br /> On the other hand, analysis of anti-rubella IgG titers in moderate and severe COVID-19 patients showed increased levels of rubella IgG in severe patients. To argue that the increase in rubella antibodies in severe COVID-19 was not due to a generalized increased antibody response, the authors mentioned that there was no increase in varicella zoster virus antibody titers in a small subset of patients analyzed. While increase of anti-rubella IgM was not clearly observed in both severe and mild patients, anti-rubella IgG antibody titers were increased in patients who had been admitted for a period of less than 7 days. The authors suggest that IgG titers trend with disease burden on the basis of the shared homology between SARS-CoV2 and rubella virus.<br /> Critical analysis of the study: <br /> This study demonstrated shared homologies between SARS-CoV2 and MMR viruses that could support the hypothesis that previous MMR vaccination protects against fatality in COVID-19 patients. The authors suggested that older populations and males were less likely to be seropositive for rubella and this might be related to their higher mortality rate. On the other hand, they found that anti-rubella IgG was higher in severe patients than mild patients with COVID-19. Since there was no information about the demographics of severe and mild patients, especially the percentage of male patients and average age to analyze the relationship between severity and MMR vaccination history, the data appears inconclusive. Because of the homology in spike protein of SARS-CoV-2 and F protein of paramyxoviruses, which are important for virus entry in the host cells, measuring cross-reactive anti-measles and anti-mumps antibody titers may provide more information on whether MMR vaccination has the potential to protect against COVID-19. <br /> The importance and implications for the current epidemics<br /> The homology search for conserved domains among different virus strains and vaccine antigens may provide helpful information to develop vaccine antigens that elicit cross-reactive immunity to several viruses. While it is not clear at present if MMR vaccination reduces or not the severity of COVID-19, given the high coverage of MMR vaccination and the potential for vaccines to modulate innate immunity, this question deserves further investigation.

    1. On 2021-04-23 10:30:29, user Paul-Olivier Dehaye wrote:

      Following criticism that the results announced do not match the data (for instance at<br /> https://pdehaye.medium.com/...<br /> or<br /> https://lasec.epfl.ch/peopl... )

      the main author seems to now (2021.04.21) acknowledge problems.

      From https://www.youtube.com/wat... :

      “What I also need to mention here is... We do see this time advantage [but] this is also early[?] days. We have not been able to dissect each and every secondary survey. This is still ongoing, but what is kind of confusing is that about 8 of those 43 specifically mentioned that they received the exposure notification before they were called up by manual contact tracing. So there is an accumulation of those people in those groups but then you still have a few [sic, given it’s 35/43!?] where manual contact tracing was first and then exposure notification was second. So the picture is still a bit blurry, but overall I think we are getting closer and we are doing additional analysis”.

      Note that, in accordance to the "Data/Code" section presented on medrxiv ("We are open to sharing individual participant data that underlie the results reported in this article, after de-identification upon reasonable requests to the corresponding author. Data requestors will need to sign a data access agreement."), the author of this comment has requested access to the data, but his request has not been acknowledged.

    1. On 2020-12-13 20:05:53, user Peter Hodgkinson wrote:

      The paper advocates an age-based priority system but then gives top priority to care homes - not the same thing! In several places it claims that this approach yields the best benefits based on the QALY method....and yet it provides no supporting math. I'll try to help out. Care home residents survive an average of 30 months from arrival so, those being immunized now will, on average survive 15 months. So the year factor equals 1.25. This figure then needs to be multiplied by a quality factor ranging from zero (no life quality restored) to one (full quality of life restored). I would like to know what figure was used?<br /> R is hovering around '1' and the ensuing lockdowns have had an awful effect on the quality of life on the rest of the 68,000,000 population. So let's work out a QALY figure for the loss of quality life over the last 9 months. The math is obvious. The vaccines should be targeted at keeping R below '1' by targeting the main 'mixers'. These are generally the people going about their daily work and this would benefit everyone. They've done this for healthcare staff - no problem with that. But why not all the many trades that are necessarily visiting peoples houses on a continuous basis?

    1. On 2021-07-30 00:51:33, user Les Campbell wrote:

      Your method seems insecure.<br /> Firstly there were no vaccinations during your “wild type “ period. There were during your alpha and delta periods. How have you controlled for this? Have you considered findings in USA and Israel that vaccine adverse reactions have influenced your results?<br /> Secondly just because you have defined periods when variants were of concern it does not follow that the women in your study had that variant without sequencing for each subject. <br /> Thirdly why do you recommend that pregnant women should get the vaccine? Women of child bearing age are at very small risk of death or severe complications. <br /> What were the cohort numbers? Especially for the delta variant? <br /> Why were no pregnant women treated with therapeutics or given simple vitamins and minerals or antibiotics (pneumonia) as they would be in many other countries?

    1. On 2020-04-12 08:33:12, user tsuyomiyakawa wrote:

      Thanks, everyone, for your precious comments.

      1. We are examining the potential confounders, which includes the ones mentioned here.

      2. As Rosemary mentioned, BCG is an attenuated version TB and, indeed, big protective effect of TB prevalence against COVID-19 exists. We will incorporate the data in the next version.

      3. We obtained the data from the web site of European Centre for Disease Prevention and Control, and are re-analyzing the growth of spreading in a more quantitive manner. Basically, there are significant effects of BCG/TB against COVID-19 growth, which will replace the data shown in Figure 3.

      4. Regarding the tourists from China, according to a survey, the top 10 destination countries of China’s out bound countries are Japan, Thailand, South Korea, Indonesia, Singapore, Malaysia, Australia, UK, New Zealand, and Maldives, and 9 out of 10 of them are the ones with extremely low COVID-19 cases and deaths (4 or lower deaths per million) , as of April 13th, which makes it unlikely that the Traveling activity from China matters. This will be added to the discussion. Also, we evaluated the number of international arrivals in each country and it did not essentially affect the results (almost at all).

      5. As for masks and green tea, they cannot explain 1) the differences between Eastern Europe and Western Europe and 2) low COVID-19 indices in Africa, South America and South East Asia. We may consider their potential effect, once we can get any good statistics representing those things, but so far, we set priority low for these potential confounders.


      Anyway, we will upload next version sometime in next week and it will be appreciated if you could keep providing us critical comments, which will greatly improve our manuscript. Thank you!

    1. On 2020-05-19 06:40:04, user Mike Stevens wrote:

      You’ve resubmitted this, but it isn’t any better.<br /> You haven’t even shown a correlative relationship, let alone a causative one.

    1. On 2020-04-01 18:46:10, user Miklos Kertesz wrote:

      Does this modeling shed any light on the approximate number of those who have been infected, and are now presumably immune?<br /> Your curves fall off quite fast. Is this realistic?

    1. On 2021-01-19 15:51:45, user Alter Ego wrote:

      In the text it is written: "LamPORE reliably detected SARS-CoV-2 to 20 copies/ml of sample. SARS-CoV-2 reads were detected in the 0.2 copies/ml sample but this was below the threshold for calling as positive sample in LamPORE but were not detected via RT-qPCR (Table 1, Figure 3)." - I assume that with "sample" the original saliva or NP sample is meant. If this is true the assay would be amazing .... my question: ins't there an error and it should be written 20 copies/microliter ... and also 0.2 copies/microliter. This would better fit to the rather low sensitivity of the assay in Figure 4 and an overall performance that is rather on the lower side of other LAMP reports where generally a cut of of approx CT=30 has ben reported (corresponding to approx 20'000copes/millilitre. This Figure is otherwise consistent with the idea that the N2 priers are much better than the E1 and ORF1ab primers....

    1. On 2021-12-29 01:27:15, user lowell2 wrote:

      conclusion? "in Omicron cases, these findings highlight the need for massive rollout of vaccinations and booster vaccinations." how so? if the vaccines DO NOT WORK, how is massive rollout going to help? vaccines every 3 months? every month? every day? The findings indicate the vaccines need to be adjusted to function better -- to actually provide IMMUNITY for a significant period of time. Not that one needs to continually use something that is ineffective.

    1. On 2020-07-30 23:36:10, user Ralph London wrote:

      How did that abstract get published??? 'magnesium 150mg OD and vitamin B12 500mcg' - in what form was the magnesium and what vitamer: cyanocobalamin, hydroxocobalamin, adenosylcobalamin or methylcobalamin, or combo? It matters.

    1. On 2020-04-18 06:11:39, user Sergey Morozov wrote:

      The manuscript provides the readers with the results of retrospective analysis of different regimens of treatment of SARS-Co-V2 infected patients in a single centre in Wuhan, China.<br /> Despite several limitations, properly discussed by the authors, the described results are very actual and may impact clinical practice as COVID-19 pandemic has not yet reached its peak in most of countries, no universal and highly effective treatment was found, whereas some of the proposed remedies showed their efficacy in-vitro only. The study is methodologically correct. However, if possible, I would suggest to add the information on whether selection criteria for study population were applied (all patients admitted to the hospital and who received interferon (IFN), IFN+ Umifenovir (ARB), or ARB treatment, or only some of them).<br /> The authors convincingly proved that inhaled IFN-?2b affect 2 major ways of pathogenesis, namely, viral replication and host's immune response (IL-6), while effects of ARB remain questionable.<br /> A pilot nature of the study requires confirmation of the results in randomized controlled multicentre trials with greater number of patients enrolled. Still, at the present state it may let to avoid waste of the financial sources to the treatment regimens that seem to have poor clinical effect. <br /> Minor remark: please, consider avoidance of the use of the trade name of investigated product (arbidol), if possible. The paper is very well-organized, every statement is logical, weighed and supported with objective grounds.<br /> COI statement: I have no conflict of interest in the regard to this review.

    1. On 2020-05-23 23:07:44, user Hilda Bastian wrote:

      I think it's critical that the author's co-authorship of one of its included studies be added to the disclosures, including noting that when some of them being controversial is mentioned. I have written other comments after initial review in this post: http://hildabastian.net/ind...

    1. On 2021-08-27 02:16:17, user Tom Hennessy wrote:

      Phlebotomy.

      "Reduction of the body iron stores can improve hyperandrogenemia and insulin resistance"<br /> "phlebotomy with consecutive reduction of body iron stores lowered blood pressure and resulted in improvements of markers of cardiovascular risk and glycemic control."<br /> "blood donation may prevent not just diabetes but also cardiovascular disease"<br /> “Our findings suggest that lower-end normal Hb levels are favorable for and maintenance of healthy metabolism involving mild chronic activation of the hypoxia response. Therefore modulation of Hb levels could serve as a novel strategy towards treatment of metabolic syndrome”<br /> “Our findings suggest that an increased Hb level is a predictor of elevated serum ALT in adolescent girls with dyslipidaemia. Our study also highlights the importance of further research to establish cut-off points for Hb and its utility in diagnosing and preventing the onset of dyslipidaemia in adolescents. ”<br /> "Our findings provide in vivo evidence of a relation between hyperinsulinaemia/insulin resistance, the main variables of insulin resistance syndrome and erythropoiesis. Increased red blood cell count could be considered as a new aspect of the insulin resistance syndrome that could contribute to the increased risk of developing cardiovascular problems."

    1. On 2020-12-02 17:13:01, user Steven Luger wrote:

      s cook - i'm not sure that i've seen data to back your claim that it's a "proven fact" that covid in the home spreads much faster. I'm aware of no studies of masked in the home of all people in the family with their air circulation constantly running.it gives Looking at a building like a synagogue with a MERV 8 filter and windows and doors open, 2500 square feet for 1 hour it gives that is still surprisingly low risk

    2. On 2020-12-02 03:08:13, user Kevin M wrote:

      my wife runs an in home day care. We have 5 to 7 toddlers/infants per day. Some days she has a staff member. Children are with us 9.5 hours a day.

      It is impossible to keep 2 & 3 year olds 6 feet away. Also to try to have them wear a mask, presents major choking hazards.

      So based on these models, and i played around with Coarse Cotton, and Face Shield / No Mask. for the 5 people would be 27 minutes and 10 people 17m. Is that referencing Close contact, less than 6 feet?

      Below those numbers it says 11 people can stay 6 feet apart indefinite... And on that i used Face Shield, 0% for Efficiency.

      My thoughts are, having the same group of children here 9+ hours a day. With or without a mask/shield it doesnt matter?

      And if maybe i had adults around and we had 6... 8..10 feet distance and no mask we are at a very low risk? Base on the "Note the six-foot or two meter...

      I know this is not a 100% guide. But what are your thoughts on my scenarios?

    1. On 2020-03-21 17:15:33, user escabatum wrote:

      There's no mention of rates of smoking, underlying lung disease, or other major risk factors between groups. This seems like a pretty useless study.

    1. On 2020-04-05 22:02:35, user WhiskersInCalif wrote:

      Some are seeing math that adds up to 111% in total?<br /> That might be addressed in the final peer reviewed note or a link to <br /> help media answer this type of question.

      The issue of long term lung damage is important for COVID-19.<br /> Keep on with the hard work.

    1. On 2020-12-16 20:05:03, user Wolfgang Lins wrote:

      the authors discuss "anterior nasal (AN)" swabs, and on page 4 refer to this as:

      Participants first underwent collection of the AN-sample, using the specific nasal swab provided in the test kit of the manufacturer, according to the instructions for use, which also correspond to the U.S. CDC instructions [4]. Briefly, while tilting the patient’s head back 70 degrees, the swab was inserted about 2cm into each nostril, parallel to the palate until resistance was met at turbinates, then rotated 3-4 times against the nasal walls on each side

      First, the collection procedure described here in act matches to one in that CDC manual [4], however not to the AN collection but to the collection of Nasal mid-turbinate (NMT) specimen. That is a floppy usage of the terms AN versus NMT, and should at least been detailled when defining AN in this paper.

      Second, the paper refers to a "specific nasal swab provided in the test kit of the manufacturer" for AN collection. Three lines later they write "a separate NP-swab (provided in the manufacturer test kit) for the Ag-RDT". <br /> As of my knowledge, the "STANDARD Q COVID-19 Ag Test" of SD Biosensor/Roche comes with a single kit - a NFS-1 from Noble Biosciences Inc., which is a swab for NP.

      I think it would help this paper to identify the particular "specific nasal swab" used here to obtain the AN/NMT swab - since the conclusions of this paper make a claim that "using a professional AN-sampling kit is at least equal to....". Reference 5 with a link to a sdbiosensor IFU that refers to NP swab only does not put any more light into this.

      Such a finding without properly identifying the particular kit unnecessarily reduces the value of this work.

    1. On 2021-03-24 15:30:41, user Stephen B. Strum wrote:

      I am puzzled. The full article I found with the exact same title is different from the article found on this website. The abstracts are not the same. Here's the conclusion from the pdf I found before finding this site with the exact same title and authors:

      "Conclusion: The results of our target trial emulation match with previous findings of randomized clinical trials and observational studies, which showed no beneficial effects of hydroxychloroquine, ivermectin, azithromycin, or their combinations."

      Compare the above with the conclusions found on this site:

      "Conclusions Our study reported no beneficial effects of hydroxychloroquine, ivermectin, azithromycin. The HCQ+AZIT treatment seems to increase risk for all-cause death."

      Why is there this dicrepancy?

    1. On 2020-04-15 15:04:27, user Mehee f wrote:

      this is completely unscientific the US has a population of 335M on this basis it will have 4M cases and 100,000 fatalities by now. Also you did not compare figures with other countries there is a big variation of mortality rates between 0.5% in South Korea to 12% in Italy. It is very biased report based on all estimates and no data pure speculation.

    1. On 2020-10-14 02:40:05, user Robert Stephens wrote:

      Could it be that a more recent HCoV infection increases the likelihood of the dysfunctional 'back boost'. If such is the case then perhaps this partially explains the lower second wave CFRs seen in many European countries. Maybe the Sars-CoV-2 mitigating behaviours (distancing/ masks etc) have also reduced the incidence of HCoV infections in the preceding 6 months - thereby reducing the frequency and amplitude of the back boost.

      Dr Robert Stephens MB BS FACD

    1. On 2021-06-22 14:30:04, user ibamvidivici wrote:

      2 more questions:

      you count the number of SARS-Covid-19 from the danish data base. Are in this database only symptomatic cases? Because if there are also asymptomatic cases (as it is in Germany), this has a high impact on the result. A Virus who is infecting a human cannot see, if this human is vaccinated or not, so the infection happens, whatever the human vaccination status is. Then the PCR test resluts should be nearly the same, however the vaccination status of the case/control group.

      Table 2 shows the numbers for unvacc. and vacc. people. The time period for the unvacc. people is 54 days (=study time period). But the time period for the vacc. People is different, depends on the date when they got their vaccination. Is the different time period included in the Adjusted-VE calculations?

    1. On 2020-12-03 21:43:53, user kdrl nakle wrote:

      It could also be that association is purely coincidental. Meaning people that die more often are older people and they are also more likely to be vitamin D deficient. So you really have nothing here.

    1. On 2021-09-14 06:20:47, user Mike Hawk wrote:

      A friendly grammar edit to the study, in the abstract section. Instead of, "One possibility is that such negative outcomes...while some tend respond with empathy (feeling what others feel), others tend respond with compassion (caring about what others feel)", I suggest that it should have been "One possibility is that such negative outcomes ..: while some tend to respond with empathy (feeling what others feel), others tend to respond with compassion (caring about what others feel)."

    1. On 2020-07-18 09:34:46, user Richard Harrison wrote:

      Useful paper. Good to see physics being applied to droplets and virus particles, although conclusions re aerosols will obviously be affected by air flows in any particular room.

    1. On 2021-08-26 11:13:46, user Fran Braga wrote:

      There's an English mistake in the interpretation section "Interpretation". The sentence "Coronavac vaccinees above 55 years" is repeated

    1. On 2020-03-30 11:14:51, user Mark Pepin, PhD wrote:

      The statement claiming "positive effects" of ARBs on morbitity/mortality is invalid given the nature of their study design. It should claim association only.

    1. On 2020-05-27 12:23:28, user Ankur Shah wrote:

      Very timely research that may hopefully translate to lower infection transmission for high risk health care providers and patients

    1. On 2020-04-10 10:53:43, user supervilin wrote:

      My understanding is that 30% of people placed in low nAb category reflect inability of their plasma to neutralize those few antigens (RBD, S1, and S2 proteins) expressed on pseudo SARS-CoV-2 virus. However, this work does not rule out possibility of other neutralising Abs present in this 30% category. Using real SARS-CoV-2 virus would be one way to check for this but much harder to do.

    1. On 2025-04-30 01:56:31, user Steve Kirsch wrote:

      Why isn't every state doing this? Why isn't the CDC publishing the brand comparison using the Medicare data? This was a carefully done study that took a long time to do. The lengths they went through to do the matching was extraordinary. Retsef did that so the study couldn't be attacked. Having negative controls was excellent; so rarely do you see that in a paper. These odds ratios show the Pfizer shots are too deadly to be used; vaccines are never supposed to increase your all-cause mortality. We can only wonder if the CDC will at least warn people that the paper might be right. The CDC has ALWAYS had the data to be able to replicate this study and prove to us that the shots worked. They have access to the Medicare records and could easily replicate the study. The only study I've seen doing brand comparisons was fraudulent because they did the Cox coefficients adjustments by assuming vaccines don't increase non-COVID all-cause mortality as their negative control. So they assume away the outcome. In my view, this is the most important paper of the COVID pandemic so far because it shows that at a minimum, all papers claiming huge benefits could be wrong. One thing is for sure: both positions can't be right. There is only one truth here and this paper is consistent with the record level data in the Czech Republic which showed ACM differences by brand as well.

    1. On 2020-04-19 01:39:26, user Constantine Daskalakis wrote:

      Where do the testing data for Germany and Spain come from (Fig2)? As far as I know, <br /> they don't report total number of tests performed.

    1. On 2020-06-08 02:08:18, user Simin wrote:

      Hello from Istanbul, <br /> Not a science person but just a concerned human being. <br /> I have a question if I may. <br /> The water basin siphons mentioned in the article, are they only restroom siphons or does the research include the siphons of the kitchen basins too? <br /> The reason for my question is to figure out if the grocery cleaning habits maybe ended up any virus particles in the kitchen sinks.

      Thank you for all your efforts and kind reply if possible.

      Simin

    1. On 2020-11-19 12:50:52, user Bruno Gualano wrote:

      Thank you, Robin Whittle. <br /> Outcomes, including 25OHD levels, were assessed at baseline and on hospital discharge (please see study design and treatment). Our data show that vit D3 supplementation was capable of increasing 25(OH) levels correcting vit D (difference, 22.7 ng/mL [95% CI, 19.3 to 26.1 vs placebo] and correcting vit deficiency (only 6.7% of the patients in the vitamin D3 group exhibited 25-hydroxyvitamin D deficiency (vs 51.5% in the placebo group). However, one might argue that this increase in 25(OH) levels occurred too late to result in clinical benefits among severe, hospitalized patients. In this regard, a long-term follow-up of these patients might be interesting.

    1. On 2021-03-22 17:45:56, user Steen Hvass Ingwersen wrote:

      This is an interesting study addressing the relationship btw Ct-values for positive covid-19 tests for an individual and the risk of transmission to other individuals at the point of testing.<br /> However, a number of assumptions behind the study are not fulfilled and so, in my opinion the conclusions need major revision.<br /> The reliability of every model is dependent on the assumptions behind the model. Some of these are:<br /> • It is assumed, that the person with the “primary test” has infected the secondarily infected individuals. This is not necessarily the case based on the way data has been compiled. Only the sequence of testing has been taken into account. Other possibilities than the assumed would have been possible:<br /> o The primarily and secondarily infected individuals were infected by the same third individual outside their household.<br /> o The primary case was infected by the secondary case but was classified as primary because this individual was the first to be tested within the household<br /> o The secondary case was infected by the primary case but this happened at an earlier point than the time of testing. Thus would likely have been associated with a lower Ct-value (and thus a higher viral load) than the one obtained in the test.<br /> • It is furthermore assumed that all individuals within a household went in strict quarantaine immediately after the primary positive test result. This was not necessarily the case. <br /> All the above-mentioned sources of misclassification move the relationship between the Ct-value and the risk of transmisssion in the same direction: towards higher Ct-values being associated with transmission risk. <br /> The estimate in the study was that a Ct-value of 38 was associated with 8% probability of transfection. As shown above, this value was overestimated, and there was no attempt to evaluate the degree of bias for the estimate in the study. For this reason, this estimate should be removed from the paper.

    1. On 2022-01-13 15:00:50, user Wendi wrote:

      This is fascinating because early on a common theme of discussion in some only support groups was that of how covid seemed to have altered one's body odor.

    1. On 2020-04-24 17:20:13, user Greta Bauer wrote:

      It is not the phrasing, but the numbers. You cite an incubation period range for SARS-CoV-2 of 4.5 to 5.8 days, which is incorrect. The numbers you use are the 95% CI for the mean from the Lauer, et al. paper. Here is your sentence: "The estimate of the incubation period of SARS-CoV-2 (mean, 375.1 days; range, 4.5 to 5.8 days)(Lauer et al., 2020)is in line with those of other known 38human coronaviruses, such as SARS (mean, 5 days; range, 2 to 14 days) (Varia et al., 392003)and MERS (mean, 5 to 7 days; range, 2 to 14 days)(Virlogeux et al., 2016)."

    1. On 2020-03-20 16:01:44, user Mejie Jwano wrote:

      For this to be helpful in forecasting outside China, more detail on lockdown measures should be described, as well as test availability. Overall, this seems unhelpful in forecasting US scenarios, where the virus has previously spread undetected due to test rationing, there is no strict enforcement of lockdown measures, there are no state food deliveries to residences, there are no masks available for the general population, and there is an acute shortage of respirator masks even for doctors. The public is freely circulating in supermarkets staffed by unmasked clerks. In state sanctioned video I have viewed of Wuhan, everyone has a mask, and access to food stores and even public streets is restricted. Also, residents of Wuhan are required to log symptoms with an app, which correlates individual movement to automate exposure tracing. With such information detailed in this article, it would reduce the probability of the data being misused in forecasting US scenarios.

    1. On 2020-10-30 17:10:52, user gatwood wrote:

      I suspect there could be a strong corellation between vaccination status and following a strict adherence to all COVID anti-infection guidelines, PPE etc... Experienced and medically trained Drs and nurses more likely have been vaccinated and also are more likely to follow PPE wearing and careful anti-infection routines. Support staff (food service, assistants and claening staff) with less formal medical training and understanding of infection are probably less likely to be vacinnated and also may be less likely to carefully employ all technical anti-infection measures. Would this account for the vaccinated folks having less COVID infection?

    1. On 2020-04-12 07:46:37, user German Perez Vazquez wrote:

      I don't see patients characteristics description, nor enough methodology explanation on how to ensure patients have enough follow-up to make sure outcome death/alive is reliable. I also miss comparisons with already known ICU scores. Interesting work anyway.

    1. On 2021-01-12 21:06:13, user Ca Doctorj wrote:

      @Wayne, 14 days after dose one, vaccine efficacy is >90% compared to placebo. How high do the antibody titres need to be to prevent infection? No one knows, but one dose appear to be enough.

    1. On 2021-09-11 05:04:14, user Michael Karesh wrote:

      The original, uncorrected version of this study is being used by right-wing outlets to justify and encourage distrust of the vaccine. "People smart enough to have a Ph.D. are most hesitant." Is this what the researchers intended to accomplish? The correction is, in contrast, receiving no coverage.

    1. On 2021-02-28 04:57:17, user Frank Wolkenberg wrote:

      It would be very useful to know the criteria for testing. This is not a randomized study, which makes it difficult to understand whether the number of infected cases in the vaccinated sample is equivalent to the number of infected cases in the unvaccinated sample, or whether those individuals represent an anomaly. If this were done, it would help answer the question of to what extent the vaccines protect against infection.

    1. On 2021-12-19 07:27:34, user Ole K. Fostad wrote:

      Hi Robert,

      Thanks a lot for your response! It looks like you are making a mistake here, mixing personal protection from the vaccine with the impact on hospitalization. There are substantial indications suggesting that people are more susceptible to infection in the period immediately after vaccination than before. Such a susceptibility is seen in other vaccines, and this is also plausible and reported with the mRNA vaccines. The vaccines are designed to affect the immune system, initially possibly weakening the defense with the intent of triggering a strong response with resulting increased protection (>21 days) later.

      However, what happens in the period between the vaccine is administered and until protection is achieved, has potentially a substantial impact on hospitalization. If we make the assumption that it is possible that the vaccine increases the risk of infection during the initial period after the vaccine is administered, in real life this effect could potentially increase both the hospitalization in this group and in theory, also contribute to increasing the spread of the disease.

      You are trying to measure the outcome of a single action; administering a vaccine or not. Then you assign the outcome following the action (administering the vaccine) to the alternate action (not administering a vaccine). In the case where the outcome is unfavorable both for the vaccination action and for the alternate action, this will count double in a relative comparison of the two actions, possibly making the mistake substantial. The impact of this choice is neither discussed nor justified in your paper. You could simply quantify this effect by running the analysis both with patients with one dose <21 days before positive test assigned to the vaccinated group AND, in another run, to the unvaccinated group. If the magnitude of the difference in outcome between the runs is negligible, you will have justified your choice, if not, the issue needs to be discussed in your paper and it should be examined.

      Looking forward to your response on this!

    1. On 2020-06-09 16:22:37, user Sinai Immunol Review Project wrote:

      Title <br /> Eosinopenia Phenotype in Patients with Coronavirus Disease 2019: A Multi-center Retrospective Study from Anhui, China

      Keywords<br /> • Lymphopenia<br /> • Covid-19 severity<br /> Main Findings<br /> It was previously shown that more than 80% of severe COVID-19 cases presented eosinopenia, in a cohort of Wuhan [1]. In this preprint Cheng et al. aim to describe the clinical characteristics of COVID-19 patients with eosinopenia. In this retrospective and multicenter study, the COVID-19 patients were stratified in three groups: mild (n=5), moderate (n=46) and severe (n=8). All patients received inhalation of recombinant interferon and antiviral drugs, 50% of the eosinopenia patients received corticosteroids therapy compared to 13.8% of the non-eosinopenia patients according to the patients’ clinical presentation. The median age of eosinopenia patients was significantly higher than the non-eosinopenia ones (47 vs 36 years old) as well as body temperature (not significant). Eosinopenia patients had higher proportions of dyspnea, gastrointestinal symptoms, and comorbidities. Eosinopenia patients presented more common COVID-19 symptoms, such as cough, sputum, fatigue, than non-eosinopenia patients (33.3% vs 17.2%). Interestingly lymphocytes counts (median: 101 cells/ul) in eosinopenia patients were significantly less than in non-eosinopenia patients (median: 167 cells/ul, p<0.001). All patients within the severe group recovered and presented with similar numbers of eosinophils and lymphocytes compared with healthy individuals upon resolution of infection and symptoms. The results showed by Cheng et al. are similar to another study involving MERS-Cov [2], but is contradictory to the previous observation with infants infected with respiratory syncytial virus, where high amounts of eosinophils were found in the respiratory tract of patients [3].

      Limitations<br /> The sample size of this study (n=59) is very narrow and could bias the observations described. The authors did not thoroughly measure potential confounding effects of or control for type of treatments, which were different across the patients. <br /> It is still unclear if SARS-COV-2 infection induces eosinopenia or eosinophilia in the respiratory tract, since all reports so far showed peripheral eosinophil counts. As eosinophils antiviral response to respiratory viral infections has been shown [4], it would be important have discussed if the high inflammatory response produced by eosinophils could contribute to the lung pathology during COVID-19, especially when vaccine candidates have been tested and could induce increased amounts of eosinophils.

      Significance<br /> This study suggests that eosinophilia may be a clinical phenotype of COVID-19 that distinguishes eosinopenia patients from non-eosinopenia patients. The contribution of the present study is relevant and calls for experimental analysis to reveal the importance of eosinopenia in COVID-19.

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

      1. Du, Y., et al., Clinical Features of 85 Fatal Cases of COVID-19 from Wuhan: A Retrospective Observational Study. Am J Respir Crit Care Med, 2020.
      2. Hwang, S.M., et al., Clinical and Laboratory Findings of Middle East Respiratory Syndrome Coronavirus Infection. Jpn J Infect Dis, 2019. 72(3): p. 160-167.
      3. Harrison, A.M., et al., Respiratory syncytical virus-induced chemokine expression in the lower airways: eosinophil recruitment and degranulation. Am J Respir Crit Care Med, 1999. 159(6): p. 1918-24.
      4. Lindsley, A.W., J.T. Schwartz, and M.E. Rothenberg, Eosinophil responses during COVID-19 infections and coronavirus vaccination. J Allergy Clin Immunol, 2020.
    1. On 2021-07-27 01:29:32, user Vaskor Basak wrote:

      Thank you very much for sharing this paper. I am interested to know what lag time was assumed between infections and deaths when calculating or inferring the CFR figures. Was it possible to use a distribution of variable lag times, based on real life data, for more sophisticated modelling? Also, has the lag time increased and/or CFR decreased as new medical interventions have slowed down the rapid onset of Covid-19 for severe cases requiring hospitalisation, since the beginning of the pandemic?

    1. On 2020-05-16 16:43:20, user Itsme Forsure wrote:

      A study of 65,000 italians who took HCQ for lupus or RA revealed that 20 people had the antibodies for covid19 and NONE have severe symptoms of covid19. Someone told me the same was found in 1.5million americans, but I can't find the study.

    1. On 2020-07-26 18:05:01, user Marm Kilpatrick wrote:

      In re-reading the study, I've found a small error. In the 3rd paragraph of Intro you write: "In a report by the Centers for Disease Control and Prevention (CDC) 3, only 291 of 2572 children who were infected with SARSCoV- 2 were symptomatic, though this may be due to poor reporting."<br /> In fact, this number 291/2572 are the number cases for which CDC had any data at all on symptoms, not the number that were symptomatic. The article states:<br /> "Data on signs and symptoms of COVID-19 were available for 291 of 2,572 (11%) pediatric cases and 10,944 of 113,985 (9.6%) cases among adults aged 18–64 years (Table)."<br /> Earlier the paper makes it clear that the other cases had *missing* data for symptoms for both children and adults:<br /> "At the time of this analysis, characteristics of interest were available for only a minority of cases, including hospitalization status (33%), presence of preexisting underlying medical conditions (13%), and symptoms (9.4%)."

    1. On 2021-07-20 01:26:03, user The Davidtollah wrote:

      The CDC conducted a study just a few years ago in which various responses to pandemics were considered. Lockdowns were specifically called out as unjustified and the report advised against them. The study was on the CDC site (saw it myself). It's probably still there and anyone with any actual interest could probably find it. (I don't spoon feed the trolls.)

    1. On 2020-12-28 23:51:01, user ErikCarter wrote:

      You really ought to test for infectious virus, rather than just RNA. Otherwise you can't truthfully claim that the variant results in higher "viral load"...you've not measure viral load, you've measured RNA load. These are not the same thing.

    1. On 2022-06-22 18:31:49, user Elisabeth Bik wrote:

      I have serious concerns about the data integrity of this paper, in particular about Figures 2 and 3. Some constellations of data points in these images appear to be duplicated within or across panels, and the lowest/highest values of the X axis (which should be the same across the four panels within a figure) appear to unexpectedly vary. This paper has been published in Sleep Science in 2020, under DOI: 10.5935/1984-0063.20190133 and I have posted my detailed concerns on PubPeer at https://pubpeer.com/publica...<br /> The PubPeer entry lists other concerns about this paper as well, including concerns about the ethical approval process and the p values in Table 1, raised by PubPeer user 'Meliosma donnellsmithii'.

    1. On 2021-06-18 23:22:40, user Susan Oliver wrote:

      Good points. Another important point is they didn't do an intention to treat analysis, which is the correct way to analyse a randomised control trial. Instead they arbitrarily removed anyone who had CTs above 35 in the first two consecutive tests from the analysis. This means they were no longer comparing randomised groups so the whole analysis was invalid. And, why remove only tests above 35 when their analysis endpoint was CTs above 30. This appears to be a clumsy attempt at p-hacking from a study that showed no benefit when analysed according to its original design (i.e. viral CLEARANCE at day 6).

    1. On 2020-04-06 17:15:59, user Matheus Macedo-Lima wrote:

      It seems to me some of the countries used in this analysis are still under-testing (Brazil, USA etc). Would a more suitable dependent variable be deaths/confirmed COVID cases?

    2. On 2020-03-30 11:19:13, user zetevar wrote:

      It can be an explanation of fewer cases in childhood. The effect of the vaccination decreases in elder aged. Comparing of the number of children patients in the mentioned countries is necessary to get closer to the solution.

    1. On 2021-06-11 03:59:36, user Fisher Wright wrote:

      Are you considering looking at other hospitals' data to see if you can replicate this result in an independent data set? Thanks for reading.

    1. On 2021-12-05 11:00:28, user Professor Ritual wrote:

      I actually like the modelling idea, a noble effort - but as things move fast the data used in the study is now outdated. Please remodel for the current data: 71% senior breakthrus and 50% adult breakthrus.

    1. On 2020-07-10 00:50:41, user Savage Henry wrote:

      The phrase "No aplicable as not human samples are used." has several typos, and should instead be written "Not applicable as no human subjects were used."

    1. On 2025-06-09 09:56:48, user Chris Kirk wrote:

      Were these analyses completed using the absolute data or the relative data from each study? Using the relative data would mean that the larger body mass and the taller stature of the transwomen (male) athletes would be a confound that would invalidate the results. Please discuss.

    1. On 2020-04-23 15:54:21, user MacS wrote:

      Didn't notice this was discussed already so adding to the fray. It's well known and accepted Type O blood is also less susceptible to Malaria ( https://www.sciencedaily.co... "https://www.sciencedaily.com/releases/2015/03/150309124113.htm)") And for what it is worth, we know the Malaria drug has decent favorable results. I don't see the WHO drawing on this correlation in their study of COVID19 although they are or should have the goods on the blood type difference with Malaria and should be taking all of this into consideration in countries in Africa that have now acquired a larger group of Type 'O' blood (herd immunity?)

    2. On 2020-04-06 14:39:20, user Jason Kidde wrote:

      It would be interesting to see how blood type applies along age groups with regard to disease severity and death. If the finding is preserved across age groups, this would add muster. Additionally, I'm curious about looking into death rates and severity across geographic regions. For instance how much does blood type explain the death rates in Eastern Europe being that the type A allele is more common in this region, while the type A allele virtually does not exist in South America. Will this result in lower death rates in South America? So far Brazil has a fairly average death rate (4%) compared to other nations whereas Chile's is quite good at 0.7%. I realize that many other factors effect this, principally the testing vs true total disease as well as healthcare infrastructure.

    1. On 2021-03-06 11:40:17, user Patti wrote:

      I had Covid back in October 2020, I still hane no smell or little to no taste. The feeling in my nose is driving me nuts - I call it a vortex or the feeling I have when I take a breath is like a upside down tornado - it feels like clean air and yet sometimes burns. I have used nasal saline but doesn’t seem to do anything. Also slight blood when I blow my nose.

    1. On 2020-05-03 01:41:44, user Danny C. wrote:

      Can we get the rigor of statistical analysis for the rt-PCR tests being used currently please? So many experts here weighing in.. But what about the current tests providing the current numbers? Thanks!

    1. On 2020-07-26 11:16:28, user Rosemary TATE wrote:

      This is a very interesting paper. However, I'm not convinced of the conclusions that the lower rate of test and hospitalisation are due to gender bias. It could be just that females have milder symptoms. And indeed the analysis shows that their symptom profile is different. Have the authors considered carrying out a multivariable analysis to adjust for some of these?<br /> I would suggest changing the title and moderating the conclusions. Incidentally, this is a cross-sectional study, and this should be mentioned somewhere. I would suggest replacing the term "big data" in the title with something more meaningful - as suggested in the StROBE guidelines. where is the checklist, could you please upload.

    1. On 2021-09-14 08:36:03, user Dharshana Kasthurirathne wrote:

      one of the conclusions is that the younger people are 17 times more likely to get hospitalized if they are not vaccinated, compared to those that are fully vaccinated. however, if you think of the time period compared (jan-jul), those who were unvaccinated may have had much higher chance of encountering the virus (simply cos they were in that status for a longer time) compared to those who are fully vaccinated (who were in that status for a much smaller time period). it's safe to assume that those who are fully vaccinated (particularly younger people) changed to that status quite recently. so is it correct to do such a population wide comparison without normalizing for the time since acquiring the vaccinated or unvaccinated status?

    1. On 2021-09-27 15:22:10, user Mitch Crimson wrote:

      Can the authors release more detail on how they got their denominator value wrong?

      For such a big error, may as well publicize HOW it happened since it could be educational to other studies and researchers who will want to avoid similar mistakes.

      Thanks -Mitch

    1. On 2021-02-10 09:58:44, user ad4 wrote:

      Thank you for this thorough consideration of Knock 2020. I hope this can be influential in shifting our policy away from harmful lockdowns. I wonder if you had also considered that a) reported COVID-19 deaths are likely also to be an overestimate and b) that the IFR used in Knock (2020) is likely to be exaggerated? https://www.who.int/bulleti...

    1. On 2021-01-27 06:59:12, user Peter Hessellund Sørensen wrote:

      In the graph showing mortality vs COVID19 cases as a function of T cell imunity. In Singapore 95% of the cases were in migrant workers in their 20s and 30s. Similar problems are probably present in the other countries in the sense that the way of counting cases and deaths is not the same and different population groups are infected in different countries. <br /> Allready with Singapore removed the statistical significance of the graph has vanished.

    1. On 2021-05-17 21:44:07, user Red Lawhern wrote:

      In your paper you write

      "drug monitoring programs (PDMPs) reduce prescribing rates 8.7%, while <br /> mandatory PDMPs increase death rates from opioids 16.6%, heroin and <br /> fentanyl 19.0%, cocaine 17.3% and all drugs 10.5%"

      This phrasing seems to assert demonstrated cause and effect. It is not at all clear to me that the techniques you are applying have the capability to establish that.

      Likewise, there is an important question in this process that you do not address and I would hope you may be willing to attempt: recognizing that predominant modes of overdose mortality involve multiple legal and illegal opioids in the great majority of deaths, is the contribution of opioids prescribed by doctors to their patients (not diverted) statistically significant in the overall mortality rate due to all opioids, legal and illegal? Based on the relative rarity of addiction to medically managed prescription opioids, I would suggest that it is not.

      Your comments are invited.

    1. On 2020-03-27 13:15:49, user Joshua Gagne wrote:

      Is there an obvious explanation for why the decrease in PM2.5 would be so much larger for the other cities (18.9 ug/m3) than for Wuhan (1.4 ug/m3)? It's the opposite of my (perhaps naive) expectation.

    1. On 2020-05-19 16:06:56, user Jared Roach wrote:

      The main point of this article is really good. The more variance there is in the infectiousness of individuals, the greater the probability of complete elimination. Indeed, if there is zero variance, then elimination will never occur. This assumes a fairly simple model (e.g., SIS compartmental model). The article would benefit from a few references to classical epidemiological models that the assumptions are based on. The point about animal reservoirs in the last paragraph should be more strongly emphasized. We know this virus originally came from bats, and we know that dogs and felines can be infected. So it seems very likely that there will be animal reservoirs. This point should be emphasized, with references.

    1. On 2020-06-16 00:52:47, user Wen Minneng wrote:

      A question is really difficult to answer: Will the COVID-19 pandemic show a upward or a downward trend in the southern hemisphere in the coming winter?

    1. On 2021-04-30 11:11:21, user Kontrolletti wrote:

      I am surprised by some of the numbers in the Introduction section, specifically "...the cumulative hospitalization rate has exceeded 1300 persons per 100,000 since early 2020 (2). Hospitalized patients account for 1% of COVID-19 patients...".

      Today the source given for the cumulative hospitalization rate gives a number of 531.5 persons per 100.000 for the week ending April 24. Also today, the CDC report a number of roughly 32 million total cases reported and a number of 2.1 million total new hospitalizations, which would mean that hospitalized patients would account for 6.5% of COVID-19 patients (https://www.cdc.gov/coronav... "https://www.cdc.gov/coronavirus/2019-ncov/covid-data/covidview/index.html)").

    1. On 2022-01-13 11:53:29, user kdrl nakle wrote:

      Most of Omicron hospitalized cases are double vaccinated and most of Delta cases are unvaccinated. Meaning the authors failed to conduct multivariate analysis, of course you need some work and knowledge to do that.

    1. On 2021-01-06 22:52:53, user Ana Laura Teodoro De Paula wrote:

      Where's the funnel plot? The result can't be considered if you cite a funnel plot and don't show it.

    1. On 2020-03-09 23:09:42, user Sasha Bruno wrote:

      What was the total sample size analyzed? ...If it was solely data from “101 confirmed cases in 38 provinces, regions, and countries outside of Wuhan” that’s a statistically small sampling.

    1. On 2023-05-15 01:46:49, user japhetk wrote:

      This report is being used to promote the anti-vaccine movement.<br /> If the actual content is certain, it is indeed a concern and should be reported, but this study shows serious concerns.

      First, this study does not take into account the number of tests. Given that the relationship between the number of vaccinations and the number of tests has been reported in many areas, this is the most serious flaw in this type of study and should be noted.<br /> Second, the results in Figure 2, which anti-vaccine activists focus on, is an inappropriate analysis that, as far as the methodology is concerned, only excludes uninfected persons from the unvaccinated population. We point out that this is one of the most serious problem of the study where the intent is clear and inappropriate.<br /> Furthermore, it is an attempt to statistically separate the effect of vaccination from the effect of previous infection, but this is not an appropriate method because many studies have reported that hybrid immunization does not show additive effects.<br /> The analysis in Figure 2 should have taken into account the history of infection and vaccination in the analysis comparing those with and without bivalent booster vaccination, but there should be no bivalent booster vaccination among the unvaccinated, which means that certain variables occurred only in one group. In this sense, this analysis is inappropriate.<br /> The raw data should be presented to show how many positives occurred among the unvaccinated, 3-dose uninfected, unvaccinated infected, 3-dose infected, etc. during the study period.<br /> Finally, this study cites a study that is convenient for cherry-picking and does not control for the number of tests, but the effect of vaccination history during this period is<br /> reported in Korea, Singapore, Japan, Luxembourg, and elsewhere, consistently contradicting the authors' results. The author's study is also inconsistent with the number of positive vaccine reports from Washington State and the CDC, which likewise do not take into account the number of tests.<br /> Bejko, Dritan, et al. "Effects of bivalent Omicron-containing vaccine boosters and prior infection against SARS-CoV-2 Omicron infections in Luxembourg, September-December 2022." Population Medicine 5.Supplement (2023).<br /> Tay, Matthew Zirui, et al. "Heterologous mRNA vaccine boosters induce a stronger and longer-lasting antibody response against Omicron XBB variant." The Lancet Regional Health–Western Pacific 33 (2023).<br /> Jang, Eun Jung, et al. "Estimated Effectiveness of Prior SARS-CoV-2 BA. 1 or BA. 2 Infection and Booster Vaccination Against Omicron BA. 5 Subvariant Infection." JAMA Network Open 6.3 (2023): e232578-e232578.<br /> https://covid.cdc.gov/covid...

      All of the above make this study problematic and raise the concerns of improper statistical analysis for use in the anti-vaccine movement. We request that raw data by number of vaccinations and number of previous infections be presented. The study appears to have been published in a low impact factor journal, and if there is data on number of tests, that should also be presented.

    1. On 2025-07-24 23:50:17, user Rong Liu wrote:

      Update on the association between influenza vaccination and cardiovascular outcomes

      Dear readers,<br /> As the authors of a living systematic review on the association between influenza vaccination, cardiovascular mortality and hospitalization, (1) we want to update readers on the findings from our most recent search. The review protocol specifies updates every six months for a minimum of three years, commencing April 2022. The baseline search was conducted on 31 May 2022, with subsequent updates on 25 January 2023 and 1 September 2023. Results from these initial searches were published in Vaccine in January 2024. (1)

      The latest search, completed on 31 March 2025, identified two studies that meet the eligibility criteria for review inclusion. Both are multi-center trials conducted within a single country, with a follow-up duration of at least 12 months. A third study was excluded due to its shorter follow-up period of only six months. (2,3) The eligible studies include a China-based trial (PANDA II) enrolling patients hospitalized for heart failure, (4) and an India-based trial (FLUENTI-MI) enrolling patients with recent myocardial infarction. (5,6) In both studies, the intervention is influenza vaccination. The comparator in FLUENTI-MI is saline placebo, and standard care in PANDA II. The primary outcome in both trials is a composite of all-cause mortality and all-cause hospitalization during the locally defined influenza season.

      As of 6 June 2025, neither study has publicly available results, and therefore we are unable to update the meta-analysis at this time. Table 1 summarizes the study characteristics and expected timelines. PANDA II completed recruitment in February 2024 and is expected to report results within the next year. (4) FLUENTI-MI is projected to complete recruitment in October 2028. Given the current pace of research in this area, we believe that biannual updates are no longer necessary, and we will transition to annual updates for the next five years, starting from the date of this latest search.

      Reference <br /> 1. Liu R, Fan Y, Patel A, et al. The association between influenza vaccination, cardiovascular mortality and hospitalization: A living systematic review and prospective meta-analysis. Vaccine. 2024/02/15/ 2024;42(5):1034-1041. doi: https://doi.org/10.1016/j.vaccine.2024.01.040 <br /> 2. Liu R, Patel A, Du X, et al. Association between influenza vaccination, all-cause mortality and cardiovascular mortality: a protocol for a living systematic review and prospective meta-analysis. BMJ Open. 2022;12(3):e054171. doi:10.1136/bmjopen-2021-054171<br /> 3. Tkaczyszyn M. Vaccination Against Influenza Pre-discharge in Heart Failure. https://clinicaltrials.gov/study/NCT06725927 <br /> 4. Zhang Y, Liu R, Zhao Y, et al. Influenza vaccination in patients with acute heart failure (PANDA II): study protocol for a hospital-based, parallel-group, cluster randomized controlled trial in China. Trials. 2024/11/25 2024;25(1):792. doi:10.1186/s13063-024-08452-8<br /> 5. Roy A. Influenza Vaccine to reduce cardiovascular events in patients with recent myocardial infarction: a multicentric randomized, double-blind palcebo-controlled trial. https://trialsearch.who.int/Trial2.aspx?TrialID=CTRI/2024/05/067056 <br /> 6. Roy A, Yadav S. Influenza vaccine in cardiovascular disease: Current evidence and practice in India. Indian Heart Journal. 2024/11/01/ 2024;76(6):365-369. doi: https://doi.org/10.1016/j.ihj.2024.11.247 <br /> https://uploads.disquscdn.c...

    1. On 2020-04-24 00:57:17, user Philip Davies wrote:

      Well, well well ...

      This pre-print would make a good script for an episode of Columbo.

      The retrospective analysis, as presented, leads the reader to just one conclusion in a bazaar of many possible conclusions.

      I am even starting to have sympathy with D. Raoult and his team. I note his hot tempered response to this paper, where he lists two enormous factors that should be considered when wrestling with the data: the fact that the HCQ and HCQ & AZ cohorts were a sicker crowd (he lists lymphopenia) and that the sickest of the non-HCQ ventilated patients were then given HCQ (plus AZ in most cases) in a desperate last bid only for most to die.

      Raoult's point is certainly valid.

      We must remember that for most of the study period the use of HCQ was "ex-license" on a compassionate basis only. This means only the sickest patients got it. Remember also that this is a retrospective analysis, therefore observational. It was not run as a therapeutic trial. On the other hand, the use of AZ was already accepted (hence 30% of the non-HCQ cohort got it anyway).... although do be aware that by this time there had been quite a lot of focus on potentially dangerous QT lengthening when HCQ and AZ were used together in very sick patients.

      The HCQ cohort was, across all key determinants, the weakest and sickest group (it had the poorest prospects looking at age, ethnicity, smoking status, congestive heart failure, peripheral vascular disease, cerebrovascular disease (strokes),dementia, COPD, Diabetes (with and without complications)! ... and indeed, the HCQ and HCQ & AZ cohorts did have 100% more lymphopenia than the non-HCQ group.

      BUT, the big asymmetric issues become obvious when we look at the pre- and post- ventilator numbers.

      In terms of patients discharged without needing ventilation, the "victorious" non-HCQ group performs poorer than the 2 treated groups. This despite having a better prognostic baseline. But the results for this group change dramatically (for the better) when we look at the outcomes of ventilation. 25 ventilated patients came from this group.... but 19 of these 25 patients were then started on HCQ or HCQ & AZ after ventilation was started. It is screamingly obvious that these would be the sickest patients in that group: they were given such compassionate drugs in extremis. So having ejected 19 of 25 ventilated patients into the other cohorts, the non-HCQ group only had 3 deaths from its remaining 6 ventilated patients.

      The numbers of ventilated patients in the other cohorts (HCQ and HCQ & AZ) were thus substantially inflated with these new super-sick patients, who mostly died.

      There really can be no conclusion at all when looking at a study of this nature without knowing much more about individual clinical conditions and guiding principles behind clinician's decision making. It's still possible to make some reasonable assumptions:

      If I were Columbo?... I would say the non-HCQ cohort contained patients of extremes, with the best and worst potential. The worst would have been the very frail (malignancy and or congestive heart failure maybe ... see the stats), who probably were earmarked for 'supplemental oxygen' only from the very start. Such patients would not have been suitable for compassionate use of non proven drugs (remember, most of this came before the "emergency use" edict by FDA). This would explain the number of non-ventilated patients who died in this group (they may have been given AZ only, not being a controversial drug, but otherwise they did not get any significant interventional therapy). These patients would have had significant chronic disease and very poor obs/indices (including lymphopenia). But given that this cohort had, overall, a better starting prognosis than the other two groups, it means that the remaining patients in the group were promising candidates for survival (with better obs/indices). Such patients, not being part of a clinical trial, would not have been offered HCQ on a compassionate basis unless they got dramatically worse .... and of course, the ones who did get worse on the ventilator were started on HCQ (& often AZ as well) and thus swapped into the HCQ / HCQ & AZ cohorts.

      If we can understand that, then we might start to think that in fact HCQ & AZ is the best performing cohort with the other 2 vaguely distant. But this is being unfair to the HCQ cohort:

      The reason that a sick patient would be given one experimental drug on a compassionate basis (HCQ) but not have a rather less experimental drug further added (AZ), can really only be explained by considering risk versus benefit. A clinician would choose to use HCQ because the patient was particularly sick. The clinician would only add AZ if it was felt that this was worth the risk.... but a particularly sick patient with significant cardiovascular disease (the HCQ contained the most CVD risk) might then die of a more abrupt arrhythmia through adding yet another QT lengthening drug. I dare say the clinicians were tempted to make some "Hail Mary" plays, but we must remember, these patients were not part of an ongoing trial, these drugs were "ex-license" for compassionate use only and clinicians were still accountable for responsible actions. So for those particularly sick frail patients, it wasn't worth the risk.

      I am pretty sure that the HCQ cohort (which had pretty good pre-ventilator stats) crashed badly because it was loaded with the sickest patients .... patients that were too sick to risk adding AZ.

      So, the findings of this retrospective analysis are, in my opinion, likely to be incorrect.

      I believe I can confidently state that:

      1. The HCQ cohort started with the sickest patients and had even more of the sickest added during ventilation. Some were too sick to risk the addition of AZ to existing HCQ.
      2. The HCQ/AZ cohort also had some very sick patients (again with more additions during ventilation).
      3. The Non-HCQ cohort had the best prognosis overall from the very start (although likely a polarized mixture of the most frail and the most promising)... and then its stats got even better when it jettisoned its sickest ventilated patients into the other 2 cohorts.

      It is almost impossible to reach a conclusion from all this. BUT, the most likely finding is NOT that adding HCQ delivers a worse outcome than standard treatment. In fact, if we look at the pre-ventilator stats, the addition of HCQ might actually have provided considerable benefit to a particularly sick group of patients. Whether or not the addition of AZ to HCQ adds benefit is also unclear ... although my 'swingometer' is pointing slightly more to benefit than harm.

      Once again. I suggest that a robust study into prophylaxis and early treatment (using sensible safer doses adjusted for pulmonary sequestration) will deliver the most interesting results for CQ/HCQ.

      Dr Phil Davies<br /> Aldershot Centre For Health<br /> http://thevirus.uk

    1. On 2020-03-28 22:38:39, user Sinai Immunol Review Project wrote:

      Summary of Findings: <br /> - Prospective cohort of 67 patients, clinical specimens taken and follow-up conducted. <br /> - Viral shedding, serum IgM, IgG antibody against NP evaluated and correlated to disease severity and clinical outcome <br /> - Viral RNA levels peaked at 1 week from febrile/cough symptom onset in sputum, nasal swabs, and stool samples. Shedding ranged from 12-19 days (median ranges) and was longer in severe patients. <br /> - IgM and IgG titers stratified patients into three archetypes as ‘strong vs weak vs non-responders’. Strong responders (with higher IgM/IgG titers) were significantly higher in severe patients.

      Limitations (specific for immune monitoring <br /> - Patient cohort is small for such a study and no individuals who were asymptotic were included; thus we cannot clearly interpret antibody titer associations with disease severity without "immunity" response.<br /> - Not clear if stool RNA captured from live infection in intestine/liver or from swallowed sputum. Transmission electron microscopy (TEM) carried out on sputum samples as proof of concept, but not stools. TEM unreasonable for actual clinical diagnosis. <br /> - Several patients had co-morbidities (such as pulmonary and liver disease) that were not accounted for when tracking antibody responses. Viral kinetics and IgM/IgG titers in subsets of patients with underlying conditions/undergoing certain medication would be informative.

      Relevance (specific for immune monitoring) <br /> - Three archetypes of antibody response to SARS-CoV-2 with different disease progression and kinetics is useful to stratify patients, and for future serological tests.

      • Strong spike-IgG levels often correlate with lymphopenia and CoVID-19 disease severity (https://doi.org/10.1101/202... ), similar to macaque studies in SARS (1). It would be critical to see if anti-NP or anti-Spike IgG antibodies for SARS-CoV-2 also elicit similar detrimental effects before clinical use.

      References: <br /> 1. Liu L, Wei Q, Lin Q, Fang J, Wang H, Kwok H, et al. JCI Insight 2019; 4(4): pii: 123158. <br /> Doi: 10.1172/jci.insight.123158

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

    1. On 2025-11-11 14:07:07, user Evolutionary Health Group wrote:

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

      Here are our highlights:

      The authors applied metagenomic sequencing to samples from multiple wastewater treatment plants to characterize the diversity and abundance of antibiotic resistance genes. Using a standardized bioinformatics pipeline, they quantified ARG classes relative to total microbial DNA, and compared treatment efficiency across plants.

      They observed that water leaving the treatment plant still harbored a broad spectrum of ARGs, including multidrug-resistance genes.

      The authors describe wastewater treatment plants as both sources and potential intervention points for antibiotic resistance by emphasizing that improved engineering and coordinated antibiotic-management strategies could limit the spread of resistance genes in urban systems.

      These findings indicate that monitoring of municipal wastewater may serve as a real-time surveillance tool for community-level antibiotic resistance burden and inform outbreak preparedness.

    1. On 2020-05-13 17:48:52, user John T. wrote:

      Dr. Wyllie,

      Any updates on where this is in the peer review process and when and in which journal it may be published?

    1. On 2021-12-08 18:41:55, user Brian Mowrey wrote:

      ~18k rapid antigen tests from before Nov 8 were added to the NICD data on November 23, and are included in the results in this update per the text.

      How many positives in the Nov 23 dump were missing sample dates? Sample dates are implied not to be "complete within the data set" per the text. Hence why receipt dates were used - but "problems have been identified with accuracy of specimen receipt dates for tests associated with substantially delayed reporting from some laboratories," again per the text.

      How many with missing sample dates were scored as "reinfections" in November? 1? 100? 1000? Delayed, non-sample-dated rapid antigen tests for summer Delta infections dumped on Nov 23 could account for the entirety of the "Omicron reinfections" presented in the update, or certainly a significant portion of them.

    1. On 2021-09-08 14:41:41, user Sherri Christian wrote:

      Can you please provide details on the HD population (I assume HD stands for healthy donor)? It doesn't appear that CD24Fc treated patients were compared directly with HD. This is an important comparison, in my opinion.

    1. On 2021-06-18 07:48:44, user Tobi wrote:

      This is really interesting and needs to be considered further.

      However, such fine tuning effects upon natural infection of artificial eliciting events are - at least from my experience - not unusual, since induced reactions to a specific PAMP always lead to physiological readjustments of "the whole system" and, thus, also affect reactions to certain other immunological stimuli (no upregulations without downregulations).

      Therefore, it's a shame that this preprint is already misused by YouTubers to generate fear of COVID vaccines due to long term effects.

    1. On 2020-10-27 12:57:35, user Alexander Samuel wrote:

      Dear Le Bon,

      What elements make you state that "600mg per day is probably fine for early treatment" ? <br /> It seems not supported by any data except Gautret et al.'s scientific fraud, by comparing classical PCR (in 2/3rds of their control group) which was systematically considered as positive since it is a manual revelation of the result with qRT-PCR. When the 2/3rds of "forced positives" are removed from their data, there is no decrease of viral load compared to control, even without considering the significance issue of the small sample.

      Clinical trials and massive prescription should never have happened based on such fraudulent data, but it did. So there are scientists involved, who claimed it works while not knowing, and who then publish retrospective studies stating "it worked". These studies are not trustworthy at all. Inclusion criteria can be manipulated easily with full access to raw data.

      I am not aware of any real clinical study favoring "600 mg in early treatment" - which means something that is not a retrospective whitewashing of poor ethical conduct in hospitals worldwide, or poor understanding of Gautret et al.'s fraudulent publication and PCR data manipulation.

      Would you be so kind and quote any study i would have missed in that sense ?

      Could you also indicate what references your statement about longer delay and lower dose in immunomodulatory effect ?

    1. On 2025-07-08 12:22:49, user Md Rakibul Hasan wrote:

      The article have recently been published in a journal, please see the following link

      Hasan, M. R., Sultana, N., Panthi, S., Hasan, M., Jahan, S., & Hasanat, M. A. (2025). Fasting Plasma Glucose as a Primary Screening Test for the Diagnosis of Gestational Diabetes mellitus: Fasting Plasma Glucose and Gestational Diabetes mellitus. Journal of the Medical College for Women & Hospital, 21(1), 43–51. https://doi.org/10.3329/jmcwh.v21i1.80952

    1. On 2021-09-07 18:29:08, user Eileen Doyle wrote:

      Eugene uses a popPK model for fluoxetine concentrations in breast milk to predict systemic concentrations (the Tanoshima 2014 paper from which the model was developed states, "the objective of this proof-of-concept study was to develop a simple pop PK model predictive of FX and NFX milk concentrations without referring to plasma concentrations..."). While Tanoshima concludes that the estimates were consistent with those of the plasma/milk-based pop PK model, the authors are comparing the milk estimates, not the plasma estimates. <br /> Additionally, the author states the unbound fraction of fluoxetine is 0.94. Fluoxetine is 94.5% protein bound [Prozac(R) label], giving an unbound fraction of 5.5%.

      I have contacted the author with this comment as well.

    1. On 2020-07-18 00:08:26, user dottore b wrote:

      As an emergency physician turned co-voligist (not my choice!), this paper is one of the single most important papers of the year. Period. We need to get governments, academic institutions, payer providers and even venture capital in public-private partnerships deploying this system today