Thread by @mega_pindang71

The receptors involved in SARS-CoV-2 infection are co-expressed in the cells of the NVU, especially in astrocytes and microglial cells. These receptors are functionally active as exposure of endothelial cells to the SARS CoV-2 S1 protein subunit ..
#HIV
#ACE2
#brain

https://twitter.com/cgkrings/status/1424952985159880724

altered the expression pattern of tight junction proteins, such as claudin-5 and ZO-1. Additionally, HIV-1 infection upregulated ACE2 and TMPRSS2 expression in brain astrocytes and microglia cells.
#astrocytes
#microglia
#brain

SC2 in BBB mechanism.

SARS-CoV-2 may infect cells in the brain, at least in some more severe COVID-19 cases, and mechanisms by which it may enter the brain across the BBB.

Studies using portions of the spike VAP of SARS-CoV-2 have shown in wild-type mice that S1 can cross the intact

BBB through a mechanism of adsorptive endocytosis, suggesting that human ACE2 is not required. The olfactory route is a minimal contributor to S1 protein uptake into the brain.

SARS-CoV-2 infection may influence the functions of BECs and other components of the NVU through direct physical interactions with the virus and its proteins, or through inducing host factors such as cytokines.

It is plausible that both mechanisms could influence long-term neurological outcomes in COVID-19 survivors.

ncbi.nlm.nih.gov/pmc/articles/P…

Astrocytes, K+ ion, Glutamate excitotoxicity (potential mechanisms for neuronal injury in several neurological diseases including ALS, Alzheimer’s disease, and HAND.
Exposure of cultured astrocytes to HIV-1 and gp120 impaired transport of extracellular glutamate by astrocytes.

HIV-1 envelope proteins gp120 and gp41 have also been shown to impair glutamate uptake by primary human astrocytes, suggesting that disruption of astrocyte glutamate transport may be a common cytopathogenic activity mediated by some neurotropic retroviruses.

ncbi.nlm.nih.gov/pmc/articles/P…