Predictors of Nonseroconversion after SARS-CoV-2 Infection, 2021, Liu et al

Hoopoe

Senior Member (Voting Rights)
Predictors of Nonseroconversion after SARS-CoV-2 Infection
https://wwwnc.cdc.gov/eid/article/27/9/21-1042_article


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CDC study finds that 36% of COVID patients never make antibodies


This has implications for prevalence studies of long covid that assume a lack of antibodies means the patient's symptoms cannot be caused by the virus.

Also interesting: age <40 years and milder illness make seroconversion less likely.
 
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So does this mean there will be some Long Covid patients being wrongly accused of never having had Covid-19 in the first place?

I'm not following this as closely but I understood long covid is more common in younger people, which are also less likely to seroconvert according to this new study. The percentage of long covid patients without antibodies could be higher than 36%.
 
FWIW I didn't make any (at approx 8 weeks; I got an antibody test as soon as available) but I was lucky in that my doctor soon realized that didn't mean I hadn't had covid. Unfortunately he's had to retire now and there are still somehow people who do not understand that we did not have PCR testing yet and that antibody tests are often negative. (FWIW I am female, under 40, had mild illness) (Edit to clarify effect it had on me: I became severe gradually in the months following having covid and still have not recovered)

I am upset at the alleged gender difference between men and women making antibodies. Seems much more common that women test negative (seems that this is also stated in this study); not enough discussion of this.
 
Interesting. There was recently an opinion piece in the New York Times that argued that long covid was psychosomatic because most patients did not show an antibody response to the coronavirus.

The authors wrote: "Antibody testing has some level of false negatives, and antibody levels can wane; however, most people with a prior infection have antibodies for some time, so such testing remains informative overall."
See: https://www.s4me.info/threads/bps-attempts-at-psychologizing-long-covid.16013/page-45#post-365048

If a large proportion of those infected with the coronavirus does not develop antibodies (as this study shows) and this subgroup without antibodies is more likely to develop long covid, then that there would be an explanation.
 
Interesting. Maybe it could boost more people within medicine to a greater portion of humility when it comes to the “unknown”, everything that can’t be seen by the eye or measured in a blood sample, although this is actually measured here on the double!

This is perfect. The irony. Patient are diagnosed with sars-cov 2 after state of the art-medicine methods, then you measure level of antibodies after gold standard-and-everything-is-fine, except it’s not, cause they don’t have antibodies, but hey they are still ill longtime after. What to make of that?

A) keep an open curious mind to the idea that there are things that medicine for many different reasons simply hasn’t figured out yet.

B) Jump to bps-like conclusions, fear/avoidance/wrong-thinking automatically, cause everything in medicine is figured out a long time ago. Period. Hmmm???
 
It would be interesting to know whether that might apply equally to other viruses. There were once cases of "atypical glandular fever" leading to ME. They were atpical in that although clinically similar to, indeed indistinguishable from, glandular fever no trace of the usual viruses could be found. I was told in 1981 that it was thought that there was a window for finding the virus and if that was missed that was it. No doubt testing moved on.
 
I wonder how some Long Covid patients apparently improving after vaccination might tie into this.

One could suspect that the lack of antibodies combined with some viral persistence (which has been demonstrated) might lead to chronic symptoms. The vaccine would stimulate antibody production and help end the stalemate, or at least reduce the persistence of the virus.
 
One could suspect that the lack of antibodies combined with some viral persistence (which has been demonstrated) might lead to chronic symptoms. The vaccine would stimulate antibody production and help end the stalemate, or at least reduce the persistence of the virus.
This hypothesis would need to be tested. Fortunately there is a lot of funding for Covid research.
 
One could suspect that the lack of antibodies combined with some viral persistence (which has been demonstrated) might lead to chronic symptoms. The vaccine would stimulate antibody production and help end the stalemate, or at least reduce the persistence of the virus.
But I wonder why a vaccine would stimulate antibody production when the virus itself wouldn't?
 
I have seroconverted and would be POS on a pos/ neg scale. But I have only a low number of antibodies and 'borderline ' T cell response.( separate test)

I don't know how to interpret this. My GP says I am immunocompromised and need a booster. So after 2 jabs which made me very ill for months, I have to start again.
 
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