Chris Turnbull
@ EnemyInAState11 avr. 2022
1/ New Research: HIV-like mechanism of immune system destruction found in Sars Cov 2 (Covid 19) infection.
Sars 2 has now been found to infect the immune system directly causing immune system cell death and depletion using a mechanism similar to HIV.
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Another interesting paper from China here from the now notorious team at the Wuhan Insititute of Virology (WIV).
The researchers have investigated how the virus causes marked lymphopenia: a condition where our white blood cells that are essential for fighting viruses and...
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...bacteria are found to be significantly reduced: thus making it much harder to fight off infections.
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They wanted to find out if the mechanism for this was as a direct result of the virus infecting the white blood cells (lymphocytes), rather than just the result of the body fighting a viral infection—something which is known to cause low...
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... white blood cell counts in pretty much all viral infections during the acute phase for a short period of time until recovery.
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What they found is that the Sars 2 directly infects the lymphocytes (white blood cells) themselves using a mechanism that is also known in HIV to cause immune system damage and kill vital immune system cells known as CD4s...
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...the destruction of the CD4 cells in HIV is partly what leads to the development of AIDS.
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The researchers demonstrated that the Sars 2 white blood cells were not only infected but also destroyed in a process known as apoptosis: showing that the virus infects this viral arm of the immune system and then kills it.
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The researchers also found that the mechanism by which the virus infects the immune system cells is also similar to that of HIV: they found that it infects the T-cells not through the 'usual mechanism' of ACE2/TMPRSS2 receptors...
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...but rather through LFA-1 which is a known binding route seen in also in HIV.
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The Authors conclude that:
'Here, we showed that SARS-CoV-2 infected T lymphocytes, mainly CD4 + T cells, in an ACE2-independent manner. SARS-CoV-2 infection triggered pronounced T-cell death, which potentially contributed to lymphopenia in patients with COVID-19..
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... T-cell infection may also pose profound influences on patients. Infected T lymphocytes not only lost the ability to control viral infection but may also carry viruses to other parts of the body through blood circulation. In addition..
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...this ACE2-independent infection mode may compromise the therapeutic effect of neutralizing antibodies targeting at spike-ACE2 binding. These may synergistically result in more severe infection outcomes in patients with COVID-19.'
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And:
'It has been debated whether SARS-CoV-2 impaired the functionality of immune cell populations through direct infection. Our results provided evidence to show that SARS-CoV-2-infected T cells, as viral RNA, viral sgRNA, viral protein, and the infectious virus could...
...be detected from T cell upon infection or from patient PBCs, although the production of infectious virus particles may stay at a low level. Several recent studies also revealed that multiple immune cells carry viral antigen or viral RNA, including neutrophils, macrophages..
... inflammatory monocytes, plasma B cells, T cells, and NK cells through postmortem histology analysis and single-cell/single-nuclear RNA-seq to lung or BALF. This suggests that SARS-CoV-2 should have a broad tropism of target cells, including major immune cells populations.'
In this study they looked at patients with severe infection only (the easiest to study)—however, the mechanism they've found may well apply to all Sars 2 infection.
The study also shows, yet again, that reliance on just spike and just ACE2 for virus entry is not correct: time to move beyond that now.
https://www.nature.com/articles/s41392-022-00919-xSo if you want a viral part of your immune system destroyed then keep getting infected with Covid.
lol, Freudian slip **vital** part.
The so-called latent or a-symptomatic state of HIV which lasts around 10-15 years comes to mind when reading this kind of research on Sars 2.
'HIV-1 can establish a state of latent infection at the level of individual T cells. Latently infected cells are rare in vivo and appear to arise when activated CD4+ T cells, the major targets cells for HIV-1...
..which is nonpermissive for viral gene expression. Because latent virus resides in memory T cells, it persists indefinitely even in patients on potent antiretroviral therapy. This latent reservoir is recognized as a major barrier to curing HIV-1 infection.'
Extremely interesting: has potential implications for Sars Cov 2, especially given the new research:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC32344'The spike protein, often called the S1 protein, dictates which cells the virus can enter. Usually, the virus does the same thing as its binding protein, said lead author William A. Banks, a professor of medicine at the University of Washington School of Medicine...
... and a Puget Sound Veterans Affairs Healthcare System physician and researcher. Banks said binding proteins like S1 usually by themselves cause damage as they detach from the virus and cause inflammation'
'The S1 protein likely causes the brain to release cytokines and inflammatory products,” he said'
'Banks and his team saw this reaction with the HIV virus and wanted to see if the same was happening with SARS CoV-2.
Banks said the S1 protein in SARS-CoV2 and the gp 120 protein in HIV-1 function similarly. They are glycoproteins – proteins that have a lot of sugars on them..
... hallmarks of proteins that bind to other receptors. Both these proteins function as the arms and hand for their viruses by grabbing onto other receptors. Both cross the blood-brain barrier and S1, like gp120, is likely toxic to brain tissues.'
'It was like déjà vu,” said Banks, who has done extensive work on HIV-1, gp120, and the blood-brain barrier.
The Banks’ lab studies the blood-brain barrier in Alzheimer’s, obesity, diabetes, and HIV. But they put their work on hold and all 15 people in the lab started their...
...experiments on the S1 protein in April. They enlisted long-time collaborator Jacob Raber, a professor in the departments of Behavioral Neuroscience, Neurology, and Radiation Medicine, and his teams at Oregon Health & Science University.'
To make it clear: none of this is to say that the virus has been created on purpose with deliberate insertions: rather I'm just illustrating that the working mechanism are plausible.
Accueil 
