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This is one of the things I've long since suspected about COVID - it attacks Mitochondria. The Mitochondria ROS pathway = the Reactive Oxygen Species pathway. Essentially, when you don't have enough oxygen, your mitochondria are able to detect that, and when they detect that, they produce an enzyme called HIF-1 (hypoxia-inducible factor 1), which then causes all your cells to behave differently. In extreme cases, it causes your cells to commit suicide - a process called apoptosis. It's an EXTREME survival reaction. Basically its your cells going "whoa, we have more important systems that we need to prioritize getting oxygen into first, before white blood cells," like the brain, and heart and vital organs. Remember when I said I lost quite a bit of hair following my severe COVID infection? Same idea. The body prioritizes certain systems over others. In this case, it's vital organs over the immune system. WHICH IS EXTREME. If they body is saying "okay, this is bad enough that I have to give up a portion of the frontline fighters of the IMMUNE SYSTEM, while being infected" that's friggin BAD. From the report: >Compared to the 24 h group, the hypoxia-related GO pathways are significantly upregulated in 48 h group, including “PID HIF1 TF pathway”, “response to hypoxia”, “positive regulation of cell death”, and “intrinsic apoptotic signaling pathway”. It has been shown that SARS-CoV-2 infection triggers mitochondrial ROS production, which induces stabilization of hypoxia-inducible factor-1a (HIF-1a) in monocytes.16 Similarly in T cells, multiple genes involved in this oxidative stress response were upregulated: BNIP3, PFKFB3, FOS, JUN, BHLHE40, GADD45B, PDK1, and DDIT4 (Fig. 4d). To corroborate the findings in T cell lines, we conducted RNA-seq analysis to primary peripheral blood mononuclear cells (PBMCs) collected from three healthy donors and three severe COVID-19 patients. Our data showed an upregulation of cell responses to stimuli, cell death, or response to hypoxia pathways, and a down-regulation of leukocytes activation and signaling pathways, similar to the findings in the T-cell line (Fig. 4e). In summary, SARS-CoV-2 infection induced pronounced T-cell death, which is probably dependent on mitochondria ROS-hypoxia pathways. More to come:

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