Shen et al.: "ACE2-independent infection of T lymphocytes by SARS-CoV-2; confirmed that SARS-CoV-2 viral antigen could be detected in patient peripheral blood cells (PBCs) or postmortem lung T cells
by Paul Alexander
& the infectious virus could also be detected from viral antigen-positive PBCs; next prove that SARS-CoV-2 infects T lymphocytes, preferably activated CD4 + T cells in vitro; 'COVID destroys T-cells'
Thus COVID virus not only can gain entry to host cells via the spike protein, it’s receptor binding sites, ACE-2 cell surface receptors, and with the insertion of the furin cleavage site at the juncture of the S1 and S2 sub-unit, but this study showed that the virus can also gain entry to lymphocytes of the immune system (white blood cells known as T-cells). COVID virus can thus do the same thing that HIV can do to lymphocytes. I am writing another stack as to the gp120 HIV insert into the spike protein.
This opens the door to the COVID virus not only being manipulated and made in the lab by Fauci, Francis Collins, Baric (U North Carolina at Chapel Hill), Daszak (EcoHealth Alliance) and Wuhan Institute of Virology, and via insertion of the furin cleavage site, but via insertion of the gp120 HIV segment (and HIV-Gag) that allows entry to the immune cells e.g. T-lymphocytes. Not only can COVID virus infect cells but can also potentially destroy the immune system.
‘SARS-CoV-2 induced marked lymphopenia in severe patients with COVID-19. However, whether lymphocytes are targets of viral infection is yet to be determined, although SARS-CoV-2 RNA or antigen has been identified in T cells from patients. Here, we confirmed that SARS-CoV-2 viral antigen could be detected in patient peripheral blood cells (PBCs) or postmortem lung T cells, and the infectious virus could also be detected from viral antigen-positive PBCs. We next prove that SARS-CoV-2 infects T lymphocytes, preferably activated CD4 + T cells in vitro. Upon infection, viral RNA, subgenomic RNA, viral protein or viral particle can be detected in the T cells. Furthermore, we show that the infection is spike-ACE2/TMPRSS2-independent through using ACE2 knockdown or receptor blocking experiments. Next, we demonstrate that viral antigen-positive T cells from patient undergone pronounced apoptosis. In vitro infection of T cells induced cell death that is likely in mitochondria ROS-HIF-1a-dependent pathways.
Finally, we demonstrated that LFA-1, the protein exclusively expresses in multiple leukocytes, is more likely the entry molecule that mediated SARS-CoV-2 infection in T cells, compared to a list of other known receptors.
Collectively, this work confirmed a SARS-CoV-2 infection of T cells, in a spike-ACE2-independent manner, which shed novel insights into the underlying mechanisms of SARS-CoV-2-induced lymphopenia in COVID-19 patients.’