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"The cells in the bone marrow known as human hematopoietic stem/progenitor cells (HSC) highly express ACE2 and TMPRSS2, making them susceptible to SARS-CoV-2 during the initial infection.. SARS-CoV-2 RNA has been detected in the bone marrow of post-mortem samples.. PBMC (Peripheral blood mononuclear cells) lack ACE2 receptor expression and do not support productive SARS-CoV-2 infection but generate a monocyte-accentuated immune response upon stimulation with SARS-CoV-2.. productive infection in the PBMC would be demonstrated by viral hijacking in favor of glycolysis, with a decrease in mitochondrial respiration as seen in patients with acute SARS-CoV-2 infection.. these findings of altered mitochondrial function in PBMC support the residual reservoir and immune dysregulation theories of PASC pathogenesis.. reservoirs of viral RNA and proteins in HSC, upon HSC differentiation, remain in PBMC and lead to altered PBMC mitochondrial function through immune activation, sustained inflammation, and the symptoms seen in PASC. Thus, the longevity of PASC would be relative to the extent of HSC viral infiltration and related to the risk factor of viremia levels. As such, this study presents a novel cellular mechanism under the currently hypothesized mechanisms of long COVID pathogenesis." In short, SARS-CoV-2 can choke off our mitochondria. 'Altered mitochondrial respiration in peripheral blood mononuclear cells of post-acute sequelae of SARS-CoV-2 infection' https://t.co/WL0U15vHQx