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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Neuroimmune multi-hit perspective of coronaviral infection

Fig. 1

Multiple environmental hits may prime microglia to modify responsiveness to SARS-COV2 and enhance the impact upon the central nervous system (CNS). Microglial cells can become “primed” as a result of advancing age and accumulated exposure to stressors, immune insults and potential environmental toxins. All of these insults have the ability to induce pathogen-associated molecular pattern (PAMPs) and damage/danger-associated molecular pattern (DAMPs) that act upon microglia and potentially induce a state of inflammatory aging or “Inflammaging”. Subsequent exposure to the SARS-COV2 virus may then further stimulate microglia and favor an “activated” pro-inflammatory phenotype. The virus, acting through ACE2 proteins and TLR receptors, may either directly enter the CNS via olfactory nerves or indirectly act by stimulating peripheral targets in the lung, gastrointestinal or other organs. Infected CD8+ T lymphocytes appear able (albeit in a limited capacity) to enter the CNS or alternatively, soluble cytokines and other inflammatory and oxidative stress factors might secondarily impact the brain. Ultimately, such factors can interact with local microglia to orchestrate a neuroinflammatory milieu, which can impact neurons and favor sickness symptoms or in extreme situations (and with chronic activation) might contribute to neuronal pathology or conceivably, even neurodegeneration in the long run

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