From: Potential molecular mechanisms of chronic fatigue in long haul COVID and other viral diseases
Viral infection | Immune cells infected and activated | Potential mechanisms for fatigue |
---|---|---|
HHV6 | CD4+ve (infection and apoptosis) and CD8+ve T cells, NK Cells, microglia (activation) | Immunosuppression [18], autoimmune reaction (IgM abs), microglial activation and production of cytokines, Amyloid-beta [24], OPC immuration, demyelination [169] |
POWV | CD4+ve Th1 cells (proliferation), B Cell (activation), macrophage (infection and activation) | Proliferation of Th1 cells, IgM production, microglia-induced inflammation, demyelination in peripheral nerves |
EBV | B cells (infection), CD8+ve T cell activation, microglia (activation) | EBV-specific CD8 + ve T cell-induced Muscle cell apoptosis [85, 87] Reactive gliosis [170], and demyelination [89] |
HIV | CD4+ve T cells (infection) [171], macrophages and microglia (infection) | Mitochondrial permeabilization and depolarization in muscle cells, activation of inflammatory T cells, microgliosis, and demyelination |
SARS-CoV2 | Lung endothelial cells (infection), kidney cells (infection), CD4+ve T (infection) [172], CD8+ve T cells (activation and exhaustion) | Cytokine storm (IL-1b, TNF-1, IL6 etc.)[173], Glial activation [174], and T cells exhaustion. Mitochondrial impairment, Direct Infection and toxicity to neurons |