The biology of coronavirus COVID-19 - including research and treatments

My memory is rusty on all of this, but I had in the back of my head (perhaps wrongly) that circulation of IgG diminished, and that the maintenance of the capacity to produce more retreated into the lymph nodes. But I will concede that may be a different process I am thinking about.

 

This is interesting, but still "suggestive" quality evidence.

Viruses need selective pressures to mutate, perhaps social distancing measures are causing selection for increased infectivity.

 

There is an initial drop, because the high level of antibodies secreted due to stimulation during the initial acute infection phase is no longer needed. Then the IgG levels move into a maintenance phase.

 

Has anyone heard of this test and can this high specifity and sensitivity be correct?

I'd still be interested in getting tested after having been ill in spring.

https://www.cegat.de/en/diagnostics/corona-diagnostics/

Edit correction

 

Who knows, unless they provide more details. They state that it is based on 1344 samples, but compared to what? Were these in-vitro controls? PCR-confirmed samples of a convenience sample?

As such, I don't put much stock in the accuracy of quoted figures unless tested in a large community/population based study, compared to other diagnostic tests.

If you are a part of a selected sample, namely you had exposure to a COVID patient, had characteristic symptoms and then were tested, you can still have some confidence in the result if it is positive.

 

Thank you! I didn't have any known contact so I guess it's still too uncertain.

 

"SARS-CoV-2-specific T cells exhibit phenotypic features of robust helper function, lack of terminal differentiation, and high proliferative potential"
https://www.cell.com/action/showPdf?pii=S2666-3791(20)30102-6

More evidence that immunity towards SARS-CoV-2 is typical and won't magically disappear in 3-12 months.

 

https://www.youtube.com/watch?v=DVxK3YUjpSA

SLC6A20
https://www.technologynetworks.com/...ssociated-with-covid-19-susceptibility-336361
Are the SLC gene family the common factor for post viral fatigue states

 

I told somebody yesterday (when they had classic covid symptoms but test came back negative, that the swab testing for active covid 19 in the uk isnt 100% reliable so they could still have it, and that the test they use has a significant false negative rate. They responded as if i were from the moon "Dont be absurd Jem, the test is negative how can i have it if the test says i dont?!

But i thought i was correct? Can anyone confirm whether i right or wrong please, i am not good at researchng these things & too foggy to interpret papers atm anyway.

 

There are bound to be some false negatives. All it needs if for someone to slip up somewhere.
I have no idea what percentage though.

 

In the US it seems to be fairly common that people have gotten negative viral tests. One reason is it could be two weeks or more after starting to have symptoms, so it might be after the viral load drops in some people. It's a big mess.

 

There are two factors affecting sensitivity, the first is variability in sampling procedures and the second is if the test is conducted too late after the individual has started to recover, the viral load can be much lower.

https://www.bmj.com/content/bmj/369/bmj.m1808.full.pdf

 

thank you both

 

Does treatment with convalescent plasma work? Wired's Adam Rogers reports that we still don't know.

Naturally, the President intervened to announce a breakthrough treatment, overriding experts. His last breakthrough didn't hold up very well.
He has also said a deep state cabal was sabotaging vaccine development, without evidence.

My own reading is that convalescent plasma may well benefit patients if given early, but has usually been used in serious cases where immune activation is not weak, and may even be a problem.

 

"weak immune activation" leads to a lack of antibodies. I don't think this is the problem at all.

I agree the key is to be given to patients early. Given late and it will just contribute to the vascular/clotting problems seen in severe patients.

 

https://twitter.com/user/status/1299000383021256705

 

Throughout this pandemic I have been looking for things that relate to mysterious problems seen in ME/CFS which COVID-19 makes much worse. One thing I have long suspected has to do with endothelial dysfunction. Several other terms related to inflammation and microvascular leakage have also caught my eye. Just recently I saw this paper which hit several of my trigger words. I'm less interested in the gruesome late-stage consequences, than I am in the molecular causes that start the inflammatory cascade. This could result in problems that fall just short of a wide range of clinical diseases which having a major impact on patient's ability to function. This is also where you can intervene before a patient winds up in intensive case.

I believe I also saw a research paper in August which used a cell sorter (flow cytometry) to identify very specific kinds of immune cells responding to infection, and determined which kinds of responses were associated with severe disease and bad outcomes. I'd like help in finding that again.

Here I have to mention a personal problem. I lost this reference because I was confined to bed by back pain after stupidly walking into a hanging lamp. My head was not affected much, being pretty solid, but my back went out in a big way, and I've spent weeks lying down and getting better. I haven't had much time to spend upright and typing until the last few days. I'm still limiting time upright. Got to go now.