A few weeks ago, I suggested that many people, in particular in Asia, may already be immune to COVID19 Virus/SARS-CoV2 because the viruses are of the same strain of SARS-CoV1 of 2003.
Two papers seem now to provide evidence of high prevalence of COVID immunity.
The first paper demonstrates that 40-60% of the unexposed population have an COVID CD4+ T cell response. (https://www.cell.com/cell/fulltext/S0092-8674(20)30610-3)
The abstract reads:
"Importantly, we detected SARS-CoV-2-reactive CD4+ T cells in ∼40%–60% of unexposed individuals, suggesting cross-reactive T cell recognition between circulating “common cold” coronaviruses and SARS-CoV-2."
The second paper reports similar results in science (https://science.sciencemag.org/content/sci/370/6512/89.full.pdf)
"Using human blood samples derivedbefore the SARS-CoV-2 virus was discovered in 2019, we mapped 142 T cell epitopes across theSARS-CoV-2 genome to facilitate precise interrogation of the SARS-CoV-2–specific CD4+T cellrepertoire. We demonstrate a range of preexisting memory CD4+T cells that are cross-reactivewith comparable affinity to SARS-CoV-2 and the common cold coronaviruses..."
A major part of the people are resistant (already).
Article A SARS-like Coronavirus was Expected, but nothing was done t...
Yes, 40-60%! Dear Pieter Borger , you pulled up a very interesting issue.
These RNA viruses may not have long lasting memory though. The samples could be archival (dates back to SARS-Cov1), or the pandemic started and was in lag phase before we recognized it. Just possible.
Dear Dr. Borger!
YOUR endavour is important so I went out to find additional resources you can use:
1) Quan-Xin, Long et al. (2020). "Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections" June 18 2020, Nature Medicine, © 2020 Springer Nature Limited, Available at:
https://www.nature.com/articles/s41591-020-0965-6
2) ECDC (2020). "Immune responses and immunity to SARS-CoV-2", © European Centre for Disease Prevention and Control (ECDC) 2020 Available at:
https://www.ecdc.europa.eu/en/covid-19/latest-evidence/immune-responses
3) Amanda, Heidth (2020). "Studies Report Rapid Loss of COVID-19 Antibodies:
The results, while preliminary, suggest that survivors of SARS-CoV-2 infection may be susceptible to reinfection within weeks or months." June 19, 2020, © 1986–2020 THE SCIENTIST, Available at:
https://www.the-scientist.com/news-opinion/studies-report-rapid-loss-of-covid-19-antibodies-67650
4) Paul Klenermann (2020). "Antiviral Responses in Covid-19:" British Society for Immunology (BSI) Webinar Series " Connecting on coronavirus: the expert hub 3 June 2020, Available at: https://www.immunology.org/coronavirus/connect-coronavirus-webinars/bsi-webinar-antiviral-responses-in-covid-19
5) Upcoming BSI webinars (2020): https://www.immunology.org/coronavirus/connect-coronavirus-webinars
Yours sincerely, Bulcsu Szekely
I agree with Dr. Md Rabiul Alam ,
https://www.cell.com/cell/pdf/S0092-8674(20)30610-3.pdf
https://www.thehindubusinessline.com/news/science/covid-19-may-have-been-infecting-humans-since-2013-study/article31932192.ece#
Maybe I did not entirely understand the respective paper you posted but I suppose that the reactivity of the CD4+ cells is due to cross immun reactivity due to previouse infections with other "common cold" circulating coronaviruses ....
Nevertheless, this is a very important paper because it offers an explanation why so many people don't have symptoms or merely mild symptoms.
I also cited the paper you mentioned in my recent published preprint which is why I am aware of it !
I'll send you an additional paper where scientists were investigating the seroprevalence of SARS-CoV-2 Antibodies in Frankfurt am Main, Germany.
Result:
N = 1000
-> 29 positive seroreactivity (Neutralizing Antibodies)
-> 5 specimen only showed specific Antibodies for SARS-CoV-2
conclusion:
24 of the initally positive tested individuals (Screening test) appear to be cross-immune !:D Great news !
Titel of this preprint:
"Epidemiological study to detect active SARS-CoV-2 infections and seropositive persons in a selected cohort of employees in the Frankfurt am Main metropolitan area"
Stefano Raffaele Hellweg Thank you very much. That there is cross reactivity may be due to common cold coronaviruses, but since the old SARS is far more similar it could be due to the hypothesis that SARS never realy died out as it has been suggested. I think SARS=COVID and that would also explain the cross reactivity.
It seems to be a fascinating theory, with somewhat brief support, however, I would dare to ask something. Given the problems that we have presented with the performance of serological tests, in terms of efficiency, how would you confirm that this patient has immunity, and has not been exposed to SARS-COV-2 based on paraclinical findings?
Pieter Borger Jaydip Datta Md Rabiul Alam Bulcsu Szekely Stefano Raffaele Hellweg Goodwin G. Jinesh
Thank you very much for the excellent discussion.
The question of cross reactivity is important. Stefano Raffaele Hellweg has interesting data, but I agree that the cross reactivity may be from some 'normal' coronoviruses that we are exposed to, and possibly even some differences in how individuals react to the viruses and create antibodies. It is a fairly large assumption to suggest that it is a SARS virus that caused them, especially without any laboratory data to show they were present and did infect.
Robert John Wolff and Jorge Andrés Sánchez-Duque
Recently I also found a manuscript (Manuscript attached) that suggests that the SARS-CoV-2 virus is probably already circulating at least since 40 years. The Data based on some sort of genetical analysis :D What do you think about this paper ?
Additionally in this manuscript I outline the context of the timeline regarding the appearance of the SARS-CoV-2 virus in the USA:
Preprint Deep analysis of the COVID-19 pandemic: A complex interactio...
Stefano Raffaele Hellweg - I quickly scanned your article and the other article in your question. First we both should emphasize that these are both Preprints and therefore in need of being carefully reviewed. Regarding the article by the Taiwan researchers I would like to suggest that it appears from the arguments that it might have been more likely that the acquisition of new gentic combinations occuring in the Pangolin most likely circulated in the Pangolin community (or moved to bats???). It seems less likely that it jumped to humans and spread among humans for those years. Another question that should be answered is what would be appropriate names for the viruses if they are not genetically the same as the current SARS-CoV-2? Obviously a virus was around, but when did it actually become the genetic form that started the outbreak? Some of the terminology used in the article may not be the correct terms. The paper appears to me to deserve quality reviews by scientist who know much more than me about the specific type of study and with knowledge of the genomic issues.
Let me also add -the article correctly states that they are proposing a "hypothesis" which means there is little, if any, real data to support the idea. This along with the unreviewed nature of the work means as scientists WE should discuss this (and hopefully study it), but it should not be presented as having any real basis until actual research can confirm the hypothesis. Hopefully if there is confirmation, more studies might move this idea toward being a theory.
Robert John Wolff - you ask: "Another question that should be answered is what would be appropriate names for the viruses if they are not genetically the same as the current SARS-CoV-2?"
Not a single virus is the same... I think we are dealing with arbitryrily "splitting" and "lumping". I myself am more like a lumper, since we have already over 15000 Mutations including >200 indel mutations in the "novel" COVID19 virus.
When do we speak of a novel virus? For SARS-CoV2, I think, there was not much novelty--neither in behaviour and infection, nor in genetics and treatment--and thus I prefer to simply see it as a mutated/recombined SARS-CoV of 2003. Two additional genetic fingerprints support my view:
Article A SARS-like Coronavirus was Expected, but nothing was done t...
Interesting results. What of outside Asia? Are there chances of populations being protected for example in Africa??
Harriet Kivumbi I have not seen studies with african data. Would also interest me. The virus has remarkably different effects on the population of different countries. In Brasil we see a huge part of the population affected, in Urugay (neighbor country of Brasil) we hardly see anything happen. Is the virus picky?
The hypothesis of previous exposure to other more benign strains of coronaviridae, eliciting antibodies that exhibit cross-reactivity with S.CoV2, seems to be the best explanation thus far. Examining the homology ( Chapter Human Coronavirus-229E, -OC43, -NL63, and -HKU1
) , immune response maps (Article A Sequence Homology and Bioinformatic Approach Can Predict C...
), and furin cleavage sites, might offer some insight in regards to potential overlap in antigenic determinants across each of the known HCoVs - SARS-CoV-2 (NC_045512.2), HCoV-229E (NC_002645.1), HCoV-NL63 (MG772808.1), HCoV-OC43 (NC_006213.1), HCoV-HKU1 (NC_006577.2).
Vincent Paul Schmitz the homology with the furin site is interesting as it was reproted to be specific for SARSCoV2---but now it is also present in HCoVs in alpha and beta coronaviruses. Is this by descent of by accident?
Pieter Borger my apologies, allow me to clarify, the alignment is a comparison of the multibasic furin cleavage sites of HCoV-OC43, HCoV-HKU1, MERS-CoV and SARS-CoV2 (all beta) versus HCoV-NL63, HCoV-229E, SARS-CoV, and RaTG13 (alpha and beta), which do not contain a furin cleavage site.
This discussion is interesting, the way different scientists argued on this emerging issue.
I am not an immunologist, but I have been following the literature and I interpret that "cross-reactive T-cell recognition" is not equivalent to immunoprotection. It could even be involved in antibody-dependent enhancement (ADE), explaining why the infection progresses further in adults than in (less exposed to similar viruses due to shorter life) children. Am I wrong?
Thanks for invitation to this very interesting-intriguing RG open quest. Many data ... Technical Report Link between SARS-CoV/2 (COVID19) and Huanan Seafood Wholesa...
...from many source-types, shows the possibility that the stat of pandemic SARSCOV2 was not located in Wuhan Market (Dec.2019) but well before this date. Data are reviewed in the following pre.-print (submitted also to China gov.)
So the populations which hadnt come into a large contact with the first outbreak of SARS Cov1 are more susceptible to COVID 19 perhaps? Since in my country any viral diseases are accounted in general Infectious Diseases database and we havent vaccinated a single person so far,this is extremely relevant.
Alen Hamzić .-. I am not sure I understand your post. If your country had less contact with SARS it could be why you have had high numbers of cases, though you seemed to have peaked in November (maybe not celebrating Thanksgiving was advantageous). Populations will also vary on susceptibility due to many other reasons including exposure to other coronoviruses (even those not causing disease), genetics (including blood type), personal/social behaviors of the population, and certainly population density and isolation. Is the non vaccination situation simply because there are none available to the population?
@ Robert John Wolff
Exactly, we had little to no contact with first SARS, also indeed additional factors should be accounted for as You mentioned in previous post. Thanksgiving as a Holiday isnt celebrated here per se, although we did have a large diaspora and tourist entry since October and now in January (loose and everchanging state rules). Not to mention that most of statistic data is easily manipulated in the entire country (lowering or increasing numbers of positive cases to access additional funds of EU). Vaccination is slow due to complex and slow administration in both Entities (Federation and RS). First contigent should arrive in February and only around 6500 doses for medicinal staff. Will separate entities rely on COVAX system or collaborate with Russian and Chinese sources, this is not yet available for scientists let alone common citizen. Thats why research comments and input like Yours are very valuable here.
In India, there has been a rapid fall in incident and active cases. The seroprevalence done in my city has recently shown to increase from 20 to 30 to now nearly 50%. Thus, herd immunity may be setting in. A vaccination drive started 10 days back will help to achieve it faster.
Dear Dr. Borger!
You raised a highly relevant issue - this virus need continuous surveillance:
1) Ewen Callaway (2021). Fast-spreading COVID variant can elude immune responses - Evidence that a variant of the coronavirus identified in South Africa might compromise immunity sparks concerns about vaccine effectiveness. Nature 589, 500-501 (2021), 21 January 2021, Open Access:
https://www.nature.com/articles/d41586-021-00121-z
2) Jelili Olaide Mustapha et al. (2021). Understanding the implications of SARS-CoV-2 re-infections on immune response milieu, laboratory tests and control measures against COVID-19, Heliyon, Volume 7, Issue 1, January 2021, Open Access:
Article Understanding the Implications of SARS-CoV-2 Re-infections o...
Yours sincerely, Bulcsu Szekely
In instance, might check following link
https://www.bbc.com/future/article/20200716-the-people-with-hidden-protection-from-covid-19
This article titled 'Immunology is where intuition goes to die' is a worthwhile read for those who want to understand these issues better.
The Pandemic's Biggest Mystery Is Our Own Immune System - The Atlantic
https://www.theatlantic.com/health/archive/2020/08/covid-19-immunity-is-the-pandemics-central-mystery/614956/
Vaccines are currently the only way to limit the infection. But there are too many negative opinions against vaccines. Even people without primary education express opinions (negative), people who do not understand anything but are "against". False "facts" are written. This prevents all of humanity from solving this serious problem.
The problem with the Covid-19 variants is spreading rapidly and the death rate has become greater either a cause of the new variants or the increase in numbers which has become exponential. The efficacy of vaccination against these variants should be tested for new mutations.
Salwa Yammine < The efficacy of vaccination against these variants should be tested for new mutations. >
3 major variants. UK variant and South Africa (SA) variant have been tested using different vaccine. The efficacies of vaccines dropped around 10% for UK variant (see attachment). Efficacies of both Pfizer-BioNtech and Moderna vaccines also significantly dropped when they are used to against SA variant. Data have published on 2/18/2021.
The antibodies induced by common cold coronaviruses can recognize (*interact*) with SARS-CoV-2. Unforturnally, they cannot neutralize SARS-CoV-2 virus (i.e. not neutralize antibodies), according to a most recent high-profile Cell paper [1]. Also, see this report [2]: "Prior infection with common cold viruses won't protect against COVID-19. "
[1] https://www.cell.com/cell/fulltext/S0092-8674(21)00160-4#%20
[2] https://www.livescience.com/antibodies-common-cold-no-coronavirus-infection.html
Please check our slide prooving the existance of common "Zero source" of the current COVID-19 pandemic. The rest works concerning the issue can be found in my profile.
Poster Evidence from Astrobiology for COVID-19 cosmic origin
Even though national avg of my country is 21 percent, a recent covid serology surveillance in my city shows 50 % antibodies.
But duration will depend in regular monitoring.
But it is clear local variations can easliy lead to spurt of cases at any time
Thailand is s country with zero cases? How are their antibodies towards SARS-CoV-2 doing over there?
Thailand is s country with zero cases? How are their antibodies towards SARS-CoV-2 doing over there?
Thailand is s country with zero cases? How are their antibodies towards SARS-CoV-2 doing over there?
Thailand is s country with zero cases? How are their antibodies towards SARS-CoV-2 doing over there?
Thailand is s country with zero cases? How are their antibodies towards SARS-CoV-2 doing over there?
Thailand is s country with zero cases? How are their antibodies towards SARS-CoV-2 doing over there?
Thailand is s country with zero cases? How are their antibodies towards SARS-CoV-2 doing over there?
Thailand is s country with zero cases? How are their antibodies towards SARS-CoV-2 doing over there?
Thailand is s country with zero cases? How are their antibodies towards SARS-CoV-2 doing over there?
@ Voskoboinick Andrey
You have copied/pasted your answer from the following source.
Article Targets of T cell responses to SARS-CoV-2 coronavirus in hum...
Please add the original source to your answer to avoid plagiarism.
Most of the infections in COVID-19 vaccine recipients are asymptomatic (>71% within first 2 weeks of first dose, and up to >84% in second dose). Similarly the unvaccinated people in contact with vaccine recipients are more likely to have asymptomatic COVID-19 in the majority of cases.
All COVID-19 vaccinated people have reduced incidence of SARS-CoV-2 infection.
For details have a look at this article published in NEJM:
Article Incident SARS-CoV-2 Infection among mRNA-Vaccinated and Unva...
@Vokoboinick Andrey Thank you for mentioning that contributors to endeavour to reference original sources to avoid plagiarism. Well done 👏
Nineteen percent of asymptomatic COVID-19 patients become long-haulers.
The 5 most common post-COVID features in all age groups were: pain, breathing difficulties, hyperlipidemia, malaise with fatigue, and hypertension.
This report (1) is based on follow up of 1,959,982 COVID-19 patients as part of analysis of health care claims (2).
1. https://www.prnewswire.com/news-releases/nineteen-percent-of-asymptomatic-covid-19-patients-develop-long-haul-covid-301312730.html
2. A detailed study of patients with long-haul COVID
https://s3.amazonaws.com/media2.fairhealth.org/whitepaper/asset/A%20Detailed%20Study%20of%20Patients%20with%20Long-Haul%20COVID--An%20Analysis%20of%20Private%20Healthcare%20Claims--A%20FAIR%20Health%20White%20Paper.pdf
The vaccine decreases chances/severity/mortality of covid. agreed.
The multiple waves increase seroprevalence. agreed
but there are reinfections and risk of recurrent waves still persists
