Multi‐organ effects of SARS‐CoV2, more than a respiratory virus: effects on human astrocytes

The coronavirus disease-2019 (COVID-19) has led to one of the major outbreaks in modern history. The etiological agent of COVID-19 is the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). SARS-CoV-2 infects the respiratory system's epithelial cells via the angiotensin-converting enzyme 2 (ACE2) receptor, causing from non or mild symptoms to severe viral pneumonia, and in some cases, death. Based on evolving clinical evidence, it is now unfitting to label SARS-CoV-2 as just a respiratory virus, as lately, various reports substantiate its pathogenicity in other organs of the body, including the central nervous system (CNS). Despite conflicting results regarding ACE2 expression in brain tissue, the latest data show that ACE2 is robustly expressed by CNS cells, suggesting that CNS is a potential target for SARS-CoV-2 infection. Astrocytes are the most abundant glial cell type within the CNS and play a role in axon guidance and synaptic support, control the blood-brain barrier flow, and regulate neuroinflammation. To test if SARS-CoV-2 can enter into the CNS via astrocytes and then elicit adverse neurological effects, we have initiated studies to test if astrocytes express ACE2 and whether SARS-CoV-2 can infect human astrocytes via this receptor. We have found that astrocytes robustly express ACE2 at the mRNA and protein levels. We are currently testing if astrocytes are susceptible to SARS-CoV-2 infection, which could subsequently lead to neuronal damage and possibly account for some of the neurological symptoms observed in COVID-19 patients. We hope to contribute to gain insights into the mechanisms of SARS-CoV-2 infection in the CNS and its potential physiological effects with this work.