ALCOHOL CONSUMPTION ON MICROGLIAL ACTIVATION AS A RISK FACTOR FOR NEUROINFLAMMATION WORSENING IN COVID-19

COVID-19 caused by the novel coronavirus, SARS-CoV-2, caused more than 700 million confirmed cases according to the world health organization (WHO). Along with life threatening symptoms, WHO also recognized, during the peak of the pandemic, an increase in alcoholic beverages consumption by population in different countries, reported as way to deal with depression and anxiety resulting from social isolation. It is known that chronic alcohol consumption leads to neuroinflammation and is a recognized risk factor for increased susceptibility to infectious diseases, by affecting immune response. In the central nervous system (CNS) microglial cells are the main responsible for immune response mediating neuroinflammation. Under pathological conditions, microglia changes from a ramified morphology to an ameboid one, adopting a pro-inflammatory secretory phenotype and phagocytic state. SARS-CoV-2 infects human cells by binding its surface protein Spike 1 to angiotensin-2-converting enzyme (ACE-2) present in human cells. Although alcohol exposure have been demonstrated to induce microglial activation, neuroinflammation and ACE2 levels modulation, it is not known whether chronic alcohol consumption could be a risk factor to increase responsivity of microglial cells to SARS-CoV-2 infection or interaction with Spike 1 protein.