Echo Yongqi Luo , Raymond Chuen-Chung Chang , Javier Gilbert-Jaramillo
{"title":"SARS-CoV-2 infection in microglia and its sequelae: What do we know so far?","authors":"Echo Yongqi Luo , Raymond Chuen-Chung Chang , Javier Gilbert-Jaramillo","doi":"10.1016/j.bbih.2024.100888","DOIUrl":null,"url":null,"abstract":"<div><div>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the COVID-19 pandemic. After the success of therapeutics and worldwide vaccination, the long-term sequelae of SARS-CoV-2 infections are yet to be determined. Common symptoms of COVID-19 include the loss of taste and smell, suggesting SARS-CoV-2 infection has a potentially detrimental effect on neurons within the olfactory/taste pathways, with direct access to the central nervous system (CNS). This could explain the detection of SARS-CoV-2 antigens in the brains of COVID-19 patients. Different viruses display neurotropism that causes impaired neurodevelopment and/or neurodegeneration. Hence, it is plausible that COVID-19-associated neuropathologies are directly driven by SARS-CoV-2 infection in the CNS. Microglia, resident immune cells of the brain, are constantly under investigation as their surveillance role has been suggested to act as a friend or a foe impacting the progression of neurological disorders. Herein, we review the current literature suggesting microglia potentially been a susceptible target by SARS-CoV-2 virions and their role in viral dissemination within the CNS. Particular attention is given to the different experimental models and their translational potential.</div></div>","PeriodicalId":72454,"journal":{"name":"Brain, behavior, & immunity - health","volume":"42 ","pages":"Article 100888"},"PeriodicalIF":3.7000,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain, behavior, & immunity - health","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2666354624001662","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the COVID-19 pandemic. After the success of therapeutics and worldwide vaccination, the long-term sequelae of SARS-CoV-2 infections are yet to be determined. Common symptoms of COVID-19 include the loss of taste and smell, suggesting SARS-CoV-2 infection has a potentially detrimental effect on neurons within the olfactory/taste pathways, with direct access to the central nervous system (CNS). This could explain the detection of SARS-CoV-2 antigens in the brains of COVID-19 patients. Different viruses display neurotropism that causes impaired neurodevelopment and/or neurodegeneration. Hence, it is plausible that COVID-19-associated neuropathologies are directly driven by SARS-CoV-2 infection in the CNS. Microglia, resident immune cells of the brain, are constantly under investigation as their surveillance role has been suggested to act as a friend or a foe impacting the progression of neurological disorders. Herein, we review the current literature suggesting microglia potentially been a susceptible target by SARS-CoV-2 virions and their role in viral dissemination within the CNS. Particular attention is given to the different experimental models and their translational potential.