The Intrinsic Severity of SARS Cov 2

It's all about immunomodulation

One of the most serious errors in assessment of SARS Cov 2 came down to misappraisals of how it causes illness. We have seen the model of harm to tissue move from cytopathic effect to immune-mediated bystander damage. For example, a few publications have shown it is T cell mediated inflammation causing anosmia rather than the virus directly causing loss of smell. Another publication in mice shows that mice without T or B cells actually have no tissue damage. This was congruent with an early paper that found a cancer patient with no T cells and chronic infection had no symptoms or signs on xray but was producing high amounts of virus for a protracted time, at least 30 days. It seems my opinion as published in 2020, that T cells were causing the harm seen in infection, was correct.

DALL E 2

The mainstream academic community has maintained that there in nothing unique about SARS cov 2 from the common cold coronaviruses. The most recent edict of it’s non-remarkability came here.

Firstly, when Phetsoupanh published his paper in 2022 he compared the changes to the immune system that occurred after sars cov 2 with the changes to the immune system from other common viral infections. He clearly states the changes following sars cov 2 were unique. Therefore, there is a unique immunomodulation.

Now, some argue this immunomodulation and harm is a function of the virus’ novelty rather than anything intrinsic. Namely, Professor Ralph Baric delivered this hypothesis (not as a hypothesis, unfortunately) in a lecture at the beginning of the pandemic.

Some pundits, journalists, and bean-counters, are unfortunately only as informed or correct as the people they speak to. Shortly after Baric’s hypothesis was presented as fact, people argued Novelty was the cause of Severity: the end of the pandemic. This piece left no room for hypothesis or for the possibility there was an intrinsic component of the virus that could create severe illness. Rather, it was the novelty that caused severe illness. Such a proclamation left no chance for reinfections to be severe in any form. Thus, the pandemic was over.

Now, there are historical examples of why this is not the case with many viruses. Dengue can cause more severe disease on reinfection. Ebola also can reinfect and is lethal when it does. Both of these viruses have an important commonality: it is their immunomodulation which creates the severe disease. T cells are killed en masse in ebolavirus infection, yet the virus itself does not infect them. The power is in immunomodulation.

A new piece of information enters the fray. SARS Cov 2 forms immunomodulatory complexes which cause overreaction and harm. And when the T cells die in ebola, they dump inflammation-causing interferons as a departing gift. Here, we have an intrinsic piece of the virus that is absolutely not going away with reinfection. The only thing that could change would be the host’s susceptibility or the code in the virus itself. The issue of an intrinsic factor creating severity persists much as the inflammation persists when viewed via modified PET several years following infection.

So, it seems each infection with sars cov 2 is unlike that of a common cold coronavirus. I hope you, dear reader, are not among those who thought it was.

Take care,

AJ