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).