SARS-CoV-2 Virus Impact on Microglia
Microglia, which resemble macrophages and seem to be CNS immune cells, play a crucial role in preserving brain homeostasis and in the quick response to damage and inflammation (66). Microglia can be activated in response to immunological stimuli, thereby shifting from ramified to amoeboid phenotype and secreting TNF-α, IL-1, and IL-6 (67). Activated microglia are included in both the neurotoxic M1 phenotype, which contributes to neuroinflammation, and the neuroprotective M2 phenotype. Based on an increasing number of studies, the neurological system may suffer irreparable harm from dysregulation and overactivation of microglia (66, 68-70).
A patient may be more likely to experience neurological and mental issues if their microglia are activated even after they have fully recovered clinically from the infection (71). Furthermore, poor or aberrant microglial function may substantially impair cognitive abilities like judgment, decision-making, learning, and memory. Accordingly, proinflammatory activation brought on by SARS-CoV-2 infection of microglia may significantly affect the short-, moderate-, or long-term neurological and psychiatric effects of infection with SARS-CoV-2 (72).
There is evidence that SARS-CoV-2 can infect a human microglial cell line directly. The RNA-seq research findings showed that a viral infection resulted in ER stress, immunological reactions, and apoptosis in the late phase. Additionally, SARS-CoV-2 infection caused human microglia to undergo apoptosis by activating both intrinsic and extrinsic pathways. In short, in lung tissues and cell lines, SARS-CoV-2 has been demonstrated to induce intrinsic and extrinsic apoptosis (73). In a preprint study also transgenic mice were found to have microglia that were infected with SARS-CoV-2, which resulted in the ongoing death of microglia and the release of pro-inflammatory cytokines (74).