A special single-issue roundup about a blockbuster new study that probably just blew the lid off the government’s covid coverup. Strap in, this might be the most important C&C post this year.
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The puzzle pieces continue to fall into place, and a significant new puzzle piece dropped last week, in the form of a preprint published to MedRxIV on July 31st, titled “
SARS-CoV-2 Uses CD4 to Infect T Helper Lymphocytes.”
Although “just” a preprint, it features no fewer than
seventy-seven authors. And it has already gathered three positive peer reviews. Let’s start with their conclusion, and then try to unpack what it means. The study’s admittedly obscure conclusion:
We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS-CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.
Not to beat a dead horse, but CD4 cells are especially important in coordinating the immune response
against infections, and they are central to the body's ability to remember and respond to specific pathogens. However, certain viruses,
like HIV, specifically target and infect CD4 cells themselves, thereby knocking out the frontline immune response and weakening the overall immune system — which alarmingly creates increased vulnerability to other opportunistic infections.
Opportunistic infections like monkeypox, Hansen’s disease, RSV, and so on. Just to name a few, at random.
So what does all this mean, beyond a weakened immune system? The researchers speculated:
Infection of CD4+ T cells by SARS-CoV-2 could explain lymphocytopenia and dysregulated inflammatory response in severe COVID-19 patients. Moreover, from an evolutionary perspective, infection of CD4+ T cells represents an effective mechanism for viruses to escape the immune response.
In other words, the spike protein’s CD4-attacking feature seems almost
designed to avoid the human immune response. Just what you’d want in a bioweapon, for example.
Once inside the CD4 cell, the covid virus weakens and kills it, destroying part of the immune system each time it happens. Worse, this process increases systemic levels of an inflammatory cytokine called Interleukin-10 (IL-10 ), which is associated with “viral persistence,” meaning an IL-10 inflammation makes it harder for the body to clear an infection. So covid — specifically its spike protein — hits the immune system two different ways.
Ultimately, the authors conceded that we don’t know how long the effect lasts: