Study: Evolution of SARS-CoV-2 in the murine central nervous system drives viral diversification. Image Credit: Stock_Good / Shutterstock.com Multiple sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral infections have been associated with neurological complications that are potentially attributed to direct infection of the central nervous system (CNS).
A recent Nature Microbiology study compares the evolution of SARS-CoV-2 in the lungs and CNS. The pathology of COVID-19 SARS-CoV-2 is the causative agent of the coronavirus disease 2019 (COVID-19) pandemic. This virus, which replicates in lung epithelial cells, can also affect the CNS, as well as induce acute kidney injury, myocarditis, and thromboembolism.
To date, the underlying host and viral characteristics that lead to these pathologies are not well understood. The entry of SARS-CoV-2 into a host cell is mediated by the viral spike glycoprotein (S), which comprises S1 and S2 subunits at the furin cleavage site (FCS). The continual evolution of SARS-CoV-2 has led to the emergence of more infectious variants of concern (VOC).
SARS-CoV-2 VOCs typically contain mutations that influence FCS cleavage efficiency and the stability of the S1/S2 interaction. Most studies examining FCS have monitored viral load in the lungs. The dynamics of altered FCS viral variants and how these mutations alter viral tropism and disease pathogenesis remain unclear.
About the study The current study used two different mou.