Abstract
Direct viral invasion, neurodegeneration, microvascular thrombosis, neuroinflammation, and severe systemic inflammation can be the causes of post-acute-COVID-19- illness neuropathology [1-4], supported by brain parenchyma and vessel changes of possibly driven inflammation in neurons, supportive cells, and brain vasculature in COVID-19 autopsy series [5,6]. A role in persistent brain effects of SARSCoV-2 (COVID-19) may be played by an accumulation of memory T cells, a biomarker of immunosenescence in tissue injury and aging, accompanying with the decreased ability to respond to new antigens that are demonstrated in chronic low-level brain inflammation [7].
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