Conclusion. Exposure to SARS-CoV-2 can induce virus-specific T cell responses without seroconversion. T cell responses may be more sensitive indicators of SARS-Co-V-2 exposure than antibodies. Our results indicate that epidemiological data relying only on the detection of SARS-CoV-2 antibodies may lead to a substantial underestimation of prior exposure to the virus
https://www.medrxiv.org/content/10.1101/2020.06.21.20132449v1
Long story short: Majority of people exposed to COVID (including people that showed symptoms) showed measurable T-cell responses (non-specific immuno-responses to COVID) but did NOT show SARS-Cov2 antibodies.
The next line is plagiarized from Twitter (@Coronavirusgoo1) but I can't put it any better, so here it is:
This could mean mass serology tests using antibody tests are missing the majority of cases.
This would mean we are far closer to herd immunity than we thought, and would explain why worse hit places like London and New York have recovered quicker.
My note: It would also explain why there has been no increase in cases in NYC even though most of the same factors causing spikes in Phoenix and Florida apply in NY too (much more activity and relaxing distancing policies).
@sh76 saidHerd immunity without SARS-COVID 2 antibodies?
Conclusion. Exposure to SARS-CoV-2 can induce virus-specific T cell responses without seroconversion. T cell responses may be more sensitive indicators of SARS-Co-V-2 exposure than antibodies. Our results indicate that epidemiological data relying only on the detection of SARS-CoV-2 antibodies may lead to a substantial underestimation of prior exposure to the virus
https://ww ...[text shortened]... spikes in Phoenix and Florida apply in NY too (much more activity and relaxing distancing policies).
Neat trick.
@no1marauder
Whatever T-cell responses fought off SARS-CoV-2 the first time the person was exposed could presumably do the same thing the second time. Granted, we don't know how long that cross-immunity would last, but we don't know precisely how long SARS-CoV-2 antibodies last either.
@sh76 saidThis would represent something of a problem, since it would mean that people could be infected and recover without becoming immune. So mitigation strategies, in other words herd immunity strategies, are doomed to failure - it also casts doubt on the viability of vaccines. So my conclusion from this is that severe lockdown, with the intent of local virus extinction, is the only viable response.
Conclusion. Exposure to SARS-CoV-2 can induce virus-specific T cell responses without seroconversion. T cell responses may be more sensitive indicators of SARS-Co-V-2 exposure than antibodies. Our results indicate that epidemiological data relying only on the detection of SARS-CoV-2 antibodies may lead to a substantial underestimation of prior exposure to the virus
https://ww ...[text shortened]... spikes in Phoenix and Florida apply in NY too (much more activity and relaxing distancing policies).
@deepthought saidFollowed up by making travel illegal.
This would represent something of a problem, since it would mean that people could be infected and recover without becoming immune. So mitigation strategies, in other words herd immunity strategies, are doomed to failure - it also casts doubt on the viability of vaccines. So my conclusion from this is that severe lockdown, with the intent of local virus extinction, is the only viable response.
@sh76
Go herd immunity!!
This is good news, sh76. And of course, there are those among us that don't like it.
From the same article linked to in the other thread I started, just because it's interesting and speaks of serology tests:
The 96% rate of asymptomatic infection among thousands of inmates in 4 state prison systems is remarkable. Without any longitudinal data, we cannot estimate the number of presymptomatic cases. If the missing data prove to be similar to the Italian, Japanese, Greek, and New York cohorts, though, the vast majority of these persons will remain asymptomatic. Why, then, might the asymptomatic infection rate in this setting be so anomalously high?
One plausible factor could be cross-immunity imparted by the betacoronaviruses HCoV-OC43 and HCoV-HKU1, which has been proposed as a mitigating factor in the spread of SARS-CoV-2 (32). According to the U.S. Centers for Disease Control and Prevention, HCoV-HKU1 was active across the United States from late November 2019 through mid-February 2020 (33). In a locked-down congregate setting like a prison, it seems possible that contagious respiratory viruses could spread rapidly, so it would be interesting to do a serosurvey for antibodies to these betacoronaviruses. Still, 96% is very high. It would be prudent to review the source data carefully for errors.
What individual differences might account for why 2 persons of the same age, sex, and health status, for example, have idiosyncratic responses to SARS-CoV-2 infection? Why does one come through with nary a symptom, while the other lies near death in intensive care? At the moment, we simply do not know. If ever there were a need for precision medicine—for deeply and thoroughly understanding the multitudinous “-omics” that shape each of us—this is it. Perhaps there will be not just 1 therapy or vaccine for SARS-CoV-2 but versions that are individualized to maximize their efficacy.
In countries like the United States that have been hardest hit by the SARS-CoV-2 pandemic, it has been apparent for some time that the amount of testing must be significantly and rapidly increased—perhaps by an order of magnitude or more. With this new knowledge that a large proportion of those infected with SARS-CoV-2 have no symptoms, the urgency for more testing becomes even greater.
I am no biologist, but I've gathered that immune systems are incredibly complex, and antibodies are not the only way a body fights infection. There are T cells, B cells, and so on. The B cells store a memory of how to produce an antibody, I think I heard recently. Thus if antibodies are not in evidence in a person's blood, there may still be improved resistance to the virus since their immune system will "remember" how to make the appropriate antibodies the next time the virus attacks. But this is slower than having antibodies already on hand, so greater feelings of sickness may still result as the virus establishes a beachhead.