SARS-CoV-2 Virus Impact on Astrocytes
SARS-CoV-2 targets astrocytes as its primary target in the brain. It has
been proven that SARS-CoV-2 preferentially infects astrocytes over
neurons in primary and organoid cortical cultures, causing astrocyte
reactivation and non-cell-autonomous neuronal death. Furthermore, it is
found that basigin (BSG) also
known as extracellular matrix metalloproteinase inducer (EMMPRIN) or
cluster of differentiation 147 (CD147) and dipeptidyl-peptidase 4 (DPP4)
are significant SARS-CoV-2 infection-related molecular actors in
cortical astrocytes (61).
As per a study carried out by Andrews et al., infected astrocytes
exhibit heightened reactivity and cellular stress (62). In addition,
SARS-CoV-2-infected cultures show non-cell autonomous inflammatory
effects such as an increase in reactive microglia and a general loss of
neurons due to apoptosis. According to research, astrocytes may have a
significant supporting function in the regulation of brain energy,
metabolism, and the microenvironment (63). It is interesting to note
that BSG/CD147 is important for the astrocyte metabolic pathways that
support the energy requirements of neurons (64).
Kriegstein et al. also showed in a preprint published that
SARS-CoV-2 preferentially infects astrocytes over other types of brain
cells, leading to fatigue, depression and “brain fog”. The virus was
introduced to brain organoids, which are tiny, lab-grown structures that
resemble the brain. Over all other cells present, astrocytes were almost
completely infected by SARS-CoV-2 (65).
Therefore, by inducing inflammation and aberrant brain energy
metabolism, SARS-CoV-2 infection in astrocytes may indirectly result in
neuronal death.