Persistent SARS-2 infections contribute to long COVID-19, Jacobs, 2021

Andy

Retired committee member
COVID-19 is a serious disease that has infected more than 40 million people. Beside significant mortality, the SARS-CoV-2 infection causes considerable and sustained morbidity, dubbed long COVID. This paper argues that some of this morbidity may be due to a persistent systemic infection. Persistent infection is indicated by continued virus RNA shedding. The virus’ superantigen could overstimulate anti-virus immune responses, and thereby induce negative feedback loops, that paradoxically allow the virus to persist. The superantigen would induce strong immune response to any residual infection. This hypothesis suggests that clearing the virus infection completely would be an appropriate intervention against long COVID.
Open access, https://www.sciencedirect.com/science/article/pii/S0306987721000566
 
"Hypothesis". :facepalm:
From the title, I expected this to be actual evidence.

Most of the cited studies (suggesting persistence) implied that 20-30 days of shedding was 'persistent', with one that found positive results up to 63 days after the initial onset. Note that all of these studies were of acute-COVID patients.

It is possible that a prolonged initial infection could be more likely to induce LongCOVID, but that is not the same as suggesting that symptoms 9 months down the track is due to the virus remaining. If the virus is remaining after that time, it begs the question, in which tissue? (because it isn't found in circulation)
 
If the virus is remaining after that time, it begs the question, in which tissue? (because it isn't found in circulation)
I must admit I am not up on my Covid research. But if Covid is potentially securing priviledged sites in tissue, and it cannot easily be found in serum, short of biopsies (hit or miss since we've no way of knowing yet what preferred tissue might be), or autopsies (these days far from a given), there are animal studies.

I am against cruelty to animals, but there is precedent here in the Tulane studies which demonstrated Bb existed in animal tissue despite treatment, and many have extrapolated that to suggest Bb can persist in humans as well.

Maybe something similar is happening with the Covid virus. Maybe this hypothesis is meant to be a platform for controlled direct testing of tissue in...whatever.
 
Last edited:
Recent experimental research shows that cats, dogs, ferrets, fruit bats, hamsters, and tree shrews can become infected with the virus. Cats, ferrets, fruit bats, and hamsters can also spread the infection to other animals of the same species in laboratory settings.
I'm also not a fan of animal testing, but infecting some ferrets or hamsters and then, sometime later when they aren't shedding virus, checking all the tissues for virus sounds possible. The difficult question of course is whether these other animals develop post-viral fatiguing syndromes. But, surely it would be worth (carefully) trying something like this? I think it would be possible to identify animals with a PVFS from their behaviour.

Having an animal model of the disease would be such an advance.
 
Many microbes easily hide in the body and evade the immune system. Detecting antibodies in the blood is different from finding organisms.

Basic biological processes are highly conserved so it is not necessary to have an animal model of disease to help ME. They only get away with a lot of their pronouncements on MUS because it is assumed that we know how a healthy organism works but this is not true.

Once we know how it should be it will be easier to see where our bodies are going wrong.

It may be that what is going wrong for us is a process that has not been discovered yet.
 
Back
Top Bottom