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Cell. Neurosci."],"abstract":"<jats:p>At the end of 2019, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was discovered in China, causing a new coronavirus disease, termed COVID-19 by the WHO on February 11, 2020. At the time of this paper (January 31, 2021), more than 100 million cases have been recorded, which have claimed over 2 million lives worldwide. The most important clinical presentation of COVID-19 is severe pneumonia; however, many patients present various neurological symptoms, ranging from loss of olfaction, nausea, dizziness, and headache to encephalopathy and stroke, with a high prevalence of inflammatory central nervous system (CNS) syndromes. SARS-CoV-2 may also target the respiratory center in the brainstem and cause silent hypoxemia. However, the neurotropic mechanism(s) by which SARS-CoV-2 affects the CNS remain(s) unclear. In this paper, we first address the involvement of astrocytes in COVID-19 and then elucidate the present knowledge on SARS-CoV-2 as a neurotropic virus as well as several other neurotropic flaviviruses (with a particular emphasis on the West Nile virus, tick-borne encephalitis virus, and Zika virus) to highlight the neurotropic mechanisms that target astroglial cells in the CNS. These key homeostasis-providing cells in the CNS exhibit many functions that act as a favorable milieu for virus replication and possibly a favorable environment for SARS-CoV-2 as well. The role of astrocytes in COVID-19 pathology, related to aging and neurodegenerative disorders, and environmental factors, is discussed. Understanding these mechanisms is key to better understanding the pathophysiology of COVID-19 and for developing new strategies to mitigate the neurotropic manifestations of COVID-19.<\/jats:p>","DOI":"10.3389\/fncel.2021.662578","type":"journal-article","created":{"date-parts":[[2021,4,9]],"date-time":"2021-04-09T05:50:16Z","timestamp":1617947416000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":55,"title":["Neurotropic Viruses, Astrocytes, and COVID-19"],"prefix":"10.3389","volume":"15","author":[{"given":"Petra","family":"Tav\u010dar","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maja","family":"Potokar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marko","family":"Kolenc","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mi\u0161a","family":"Korva","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatjana","family":"Av\u0161i\u010d-\u017dupanc","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Zorec","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jernej","family":"Jorga\u010devski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,4,9]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"641","DOI":"10.1089\/vbz.2010.0236","article-title":"Rodents as sentinels for the prevalence of tick-borne encephalitis virus.","volume":"11","author":"Achazi","year":"2011","journal-title":"Vector Borne Zoonotic Dis."},{"key":"B2","doi-asserted-by":"publisher","first-page":"198103","DOI":"10.1016\/j.virusres.2020.198103","article-title":"Immunological co-ordination between gut and lungs in SARS-CoV-2 infection.","volume":"286","author":"Ahlawat","year":"2020","journal-title":"Virus Res."},{"key":"B3","doi-asserted-by":"publisher","first-page":"1323","DOI":"10.1007\/s11064-018-2679-4","article-title":"ACE2 in Brain Physiology and Pathophysiology: evidence from Transgenic Animal Models.","volume":"44","author":"Alenina","year":"2019","journal-title":"Neurochem. 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