Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and glial cells: Insights and perspectives.
Identifieur interne : 000624 ( Main/Exploration ); précédent : 000623; suivant : 000625Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and glial cells: Insights and perspectives.
Auteurs : Gabriele Vargas [Brésil] ; Luiz Henrique Medeiros Geraldo [France] ; Natália Gedeão Salomão [Brésil] ; Marciano Viana Paes [Brésil] ; Flavia Regina Souza Lima [Brésil] ; Flávia Carvalho Alcantara Gomes [Brésil]Source :
- Brain, behavior, & immunity - health [ 2666-3546 ] ; 2020.
Abstract
In December 2019, a pneumonia outbreak was reported in Wuhan, Hubei province, China. Since then, the World Health Organization declared a public health emergency of international concern due to a growing number of deaths around the globe, as well as unparalleled economic and sociodemographic consequences. The disease called coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel form of human coronavirus. Although coronavirus infections have been associated with neurological manifestations such as febrile seizures, convulsions, change in mental status, and encephalitis, less is known about the impact of SARS-CoV-2 in the brain. Recently, emerging evidence suggests that SARS-CoV-2 is associated with neurological alterations in COVID-19 patients with severe clinical manifestations. The molecular and cellular mechanisms involved in this process, as well as the neurotropic and neuroinvasive properties of SARS-CoV-2, are still poorly understood. Glial cells, such as astrocytes and microglia, play pivotal roles in the brain response to neuroinflammatory insults and neurodegenerative diseases. Further, accumulating evidence has shown that those cells are targets of several neurotropic viruses that severely impact their function. Glial cell dysfunctions have been associated with several neuroinflammatory diseases, suggesting that SARS-CoV-2 likely has a primary effect on these cells in addition to a secondary effect from neuronal damage. Here, we provide an overview of these data and discuss the possible implications of glial cells as targets of SARS-CoV-2. Considering the roles of microglia and astrocytes in brain inflammatory responses, we shed light on glial cells as possible drivers and potential targets of therapeutic strategies against neurological manifestations in patients with COVID-19. The main goal of this review is to highlight the need to consider glial involvement in the progression of COVID-19 and potentially include astrocytes and microglia as mediators of SARS-CoV-2-induced neurological damage.
DOI: 10.1016/j.bbih.2020.100127
PubMed: 32838339
PubMed Central: PMC7423575
Affiliations:
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INSERM U970), Université de Paris, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Paris Cardiovascular Research Center (PARCC - INSERM U970), Université de Paris, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Gedeao Salomao, Natalia" sort="Gedeao Salomao, Natalia" uniqKey="Gedeao Salomao N" first="Natália" last="Gedeão Salomão">Natália Gedeão Salomão</name><affiliation wicri:level="3"><nlm:affiliation>Laboratório Interdisciplinar de Pesquisas Médicas, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz/FIOCRUZ, Rio de Janeiro, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Laboratório Interdisciplinar de Pesquisas Médicas, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz/FIOCRUZ, Rio de Janeiro</wicri:regionArea><placeName><settlement type="city">Rio de Janeiro</settlement><region type="state">État de Rio de Janeiro</region></placeName></affiliation></author><author><name sortKey="Viana Paes, Marciano" sort="Viana Paes, Marciano" uniqKey="Viana Paes M" first="Marciano" last="Viana Paes">Marciano Viana Paes</name><affiliation wicri:level="3"><nlm:affiliation>Laboratório Interdisciplinar de Pesquisas Médicas, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz/FIOCRUZ, Rio de Janeiro, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Laboratório Interdisciplinar de Pesquisas Médicas, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz/FIOCRUZ, Rio de Janeiro</wicri:regionArea><placeName><settlement type="city">Rio de Janeiro</settlement><region type="state">État de Rio de Janeiro</region></placeName></affiliation></author><author><name sortKey="Regina Souza Lima, Flavia" sort="Regina Souza Lima, Flavia" uniqKey="Regina Souza Lima F" first="Flavia" last="Regina Souza Lima">Flavia Regina Souza Lima</name><affiliation wicri:level="3"><nlm:affiliation>Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro</wicri:regionArea><placeName><settlement type="city">Rio de Janeiro</settlement><region type="state">État de Rio de Janeiro</region></placeName></affiliation></author><author><name sortKey="Carvalho Alcantara Gomes, Flavia" sort="Carvalho Alcantara Gomes, Flavia" uniqKey="Carvalho Alcantara Gomes F" first="Flávia" last="Carvalho Alcantara Gomes">Flávia Carvalho Alcantara Gomes</name><affiliation wicri:level="3"><nlm:affiliation>Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro</wicri:regionArea><placeName><settlement type="city">Rio de Janeiro</settlement><region type="state">État de Rio de Janeiro</region></placeName></affiliation></author></analytic><series><title level="j">Brain, behavior, & immunity - health</title><idno type="eISSN">2666-3546</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In December 2019, a pneumonia outbreak was reported in Wuhan, Hubei province, China. Since then, the World Health Organization declared a public health emergency of international concern due to a growing number of deaths around the globe, as well as unparalleled economic and sociodemographic consequences. The disease called coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel form of human coronavirus. Although coronavirus infections have been associated with neurological manifestations such as febrile seizures, convulsions, change in mental status, and encephalitis, less is known about the impact of SARS-CoV-2 in the brain. Recently, emerging evidence suggests that SARS-CoV-2 is associated with neurological alterations in COVID-19 patients with severe clinical manifestations. The molecular and cellular mechanisms involved in this process, as well as the neurotropic and neuroinvasive properties of SARS-CoV-2, are still poorly understood. Glial cells, such as astrocytes and microglia, play pivotal roles in the brain response to neuroinflammatory insults and neurodegenerative diseases. Further, accumulating evidence has shown that those cells are targets of several neurotropic viruses that severely impact their function. Glial cell dysfunctions have been associated with several neuroinflammatory diseases, suggesting that SARS-CoV-2 likely has a primary effect on these cells in addition to a secondary effect from neuronal damage. Here, we provide an overview of these data and discuss the possible implications of glial cells as targets of SARS-CoV-2. Considering the roles of microglia and astrocytes in brain inflammatory responses, we shed light on glial cells as possible drivers and potential targets of therapeutic strategies against neurological manifestations in patients with COVID-19. The main goal of this review is to highlight the need to consider glial involvement in the progression of COVID-19 and potentially include astrocytes and microglia as mediators of SARS-CoV-2-induced neurological damage.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">32838339</PMID><DateRevised><Year>2020</Year><Month>09</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2666-3546</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><PubDate><Year>2020</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Brain, behavior, & immunity - health</Title><ISOAbbreviation>Brain Behav Immun Health</ISOAbbreviation></Journal><ArticleTitle>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and glial cells: Insights and perspectives.</ArticleTitle><Pagination><MedlinePgn>100127</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbih.2020.100127</ELocationID><Abstract><AbstractText>In December 2019, a pneumonia outbreak was reported in Wuhan, Hubei province, China. Since then, the World Health Organization declared a public health emergency of international concern due to a growing number of deaths around the globe, as well as unparalleled economic and sociodemographic consequences. The disease called coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel form of human coronavirus. Although coronavirus infections have been associated with neurological manifestations such as febrile seizures, convulsions, change in mental status, and encephalitis, less is known about the impact of SARS-CoV-2 in the brain. Recently, emerging evidence suggests that SARS-CoV-2 is associated with neurological alterations in COVID-19 patients with severe clinical manifestations. The molecular and cellular mechanisms involved in this process, as well as the neurotropic and neuroinvasive properties of SARS-CoV-2, are still poorly understood. Glial cells, such as astrocytes and microglia, play pivotal roles in the brain response to neuroinflammatory insults and neurodegenerative diseases. Further, accumulating evidence has shown that those cells are targets of several neurotropic viruses that severely impact their function. Glial cell dysfunctions have been associated with several neuroinflammatory diseases, suggesting that SARS-CoV-2 likely has a primary effect on these cells in addition to a secondary effect from neuronal damage. Here, we provide an overview of these data and discuss the possible implications of glial cells as targets of SARS-CoV-2. Considering the roles of microglia and astrocytes in brain inflammatory responses, we shed light on glial cells as possible drivers and potential targets of therapeutic strategies against neurological manifestations in patients with COVID-19. The main goal of this review is to highlight the need to consider glial involvement in the progression of COVID-19 and potentially include astrocytes and microglia as mediators of SARS-CoV-2-induced neurological damage.</AbstractText><CopyrightInformation>© 2020 The Authors.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vargas</LastName><ForeName>Gabriele</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Medeiros Geraldo</LastName><ForeName>Luiz Henrique</ForeName><Initials>LH</Initials><AffiliationInfo><Affiliation>Paris Cardiovascular Research Center (PARCC - INSERM U970), Université de Paris, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gedeão Salomão</LastName><ForeName>Natália</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Laboratório Interdisciplinar de Pesquisas Médicas, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz/FIOCRUZ, Rio de Janeiro, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Viana Paes</LastName><ForeName>Marciano</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Laboratório Interdisciplinar de Pesquisas Médicas, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz/FIOCRUZ, Rio de Janeiro, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Regina Souza Lima</LastName><ForeName>Flavia</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carvalho Alcantara Gomes</LastName><ForeName>Flávia</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>08</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Brain Behav Immun Health</MedlineTA><NlmUniqueID>101759062</NlmUniqueID><ISSNLinking>2666-3546</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Astrocyte</Keyword><Keyword MajorTopicYN="N">COVID-19</Keyword><Keyword MajorTopicYN="N">Coronavirus</Keyword><Keyword MajorTopicYN="N">Glial cells</Keyword><Keyword MajorTopicYN="N">Microglia</Keyword><Keyword MajorTopicYN="N">Neuroinflammation</Keyword><Keyword MajorTopicYN="N">SARS-CoV-2</Keyword></KeywordList><CoiStatement>The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>06</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>08</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>08</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>8</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>8</Month><Day>25</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>8</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32838339</ArticleId><ArticleId IdType="doi">10.1016/j.bbih.2020.100127</ArticleId><ArticleId IdType="pii">S2666-3546(20)30092-2</ArticleId><ArticleId IdType="pii">100127</ArticleId><ArticleId IdType="pmc">PMC7423575</ArticleId></ArticleIdList><pmc-dir>pmcsd</pmc-dir>
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