The neuroinvasive potential of SARS-CoV2 may play a role in the respiratory failure of COVID-19 patients.
Identifieur interne : 000A02 ( PubMed/Corpus ); précédent : 000A01; suivant : 000A03The neuroinvasive potential of SARS-CoV2 may play a role in the respiratory failure of COVID-19 patients.
Auteurs : Yan-Chao Li ; Wan-Zhu Bai ; Tsutomu HashikawaSource :
- Journal of medical virology [ 1096-9071 ] ; 2020.
Abstract
Following the severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), another highly pathogenic coronavirus named SARS-CoV-2 (previously known as 2019-nCoV) emerged in December 2019 in Wuhan, China, and rapidly spreads around the world. This virus shares highly homological sequence with SARS-CoV, and causes acute, highly lethal pneumonia coronavirus disease 2019 (COVID-19) with clinical symptoms similar to those reported for SARS-CoV and MERS-CoV. The most characteristic symptom of patients with COVID-19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously. Additionally, some patients with COVID-19 also showed neurologic signs, such as headache, nausea, and vomiting. Increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the central nervous system inducing neurological diseases. The infection of SARS-CoV has been reported in the brains from both patients and experimental animals, where the brainstem was heavily infected. Furthermore, some coronaviruses have been demonstrated able to spread via a synapse-connected route to the medullary cardiorespiratory center from the mechanoreceptors and chemoreceptors in the lung and lower respiratory airways. Considering the high similarity between SARS-CoV and SARS-CoV2, it remains to make clear whether the potential invasion of SARS-CoV2 is partially responsible for the acute respiratory failure of patients with COVID-19. Awareness of this may have a guiding significance for the prevention and treatment of the SARS-CoV-2-induced respiratory failure.
DOI: 10.1002/jmv.25728
PubMed: 32104915
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The neuroinvasive potential of SARS-CoV2 may play a role in the respiratory failure of COVID-19 patients.</title><author><name sortKey="Li, Yan Chao" sort="Li, Yan Chao" uniqKey="Li Y" first="Yan-Chao" last="Li">Yan-Chao Li</name><affiliation><nlm:affiliation>Department of Histology and Embryology, College of Basic Medical Sciences, Norman Bethune College of Medicine, Jilin University, Changchun, Jilin, China.</nlm:affiliation></affiliation></author><author><name sortKey="Bai, Wan Zhu" sort="Bai, Wan Zhu" uniqKey="Bai W" first="Wan-Zhu" last="Bai">Wan-Zhu Bai</name><affiliation><nlm:affiliation>Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Science, Beijing, China.</nlm:affiliation></affiliation></author><author><name sortKey="Hashikawa, Tsutomu" sort="Hashikawa, Tsutomu" uniqKey="Hashikawa T" first="Tsutomu" last="Hashikawa">Tsutomu Hashikawa</name><affiliation><nlm:affiliation>Neural Architecture, Advanced Technology Development Group, RIKEN Brain Science Institute, Saitama, Japan.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32104915</idno><idno type="pmid">32104915</idno><idno type="doi">10.1002/jmv.25728</idno><idno type="wicri:Area/PubMed/Corpus">000A02</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000A02</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The neuroinvasive potential of SARS-CoV2 may play a role in the respiratory failure of COVID-19 patients.</title><author><name sortKey="Li, Yan Chao" sort="Li, Yan Chao" uniqKey="Li Y" first="Yan-Chao" last="Li">Yan-Chao Li</name><affiliation><nlm:affiliation>Department of Histology and Embryology, College of Basic Medical Sciences, Norman Bethune College of Medicine, Jilin University, Changchun, Jilin, China.</nlm:affiliation></affiliation></author><author><name sortKey="Bai, Wan Zhu" sort="Bai, Wan Zhu" uniqKey="Bai W" first="Wan-Zhu" last="Bai">Wan-Zhu Bai</name><affiliation><nlm:affiliation>Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Science, Beijing, China.</nlm:affiliation></affiliation></author><author><name sortKey="Hashikawa, Tsutomu" sort="Hashikawa, Tsutomu" uniqKey="Hashikawa T" first="Tsutomu" last="Hashikawa">Tsutomu Hashikawa</name><affiliation><nlm:affiliation>Neural Architecture, Advanced Technology Development Group, RIKEN Brain Science Institute, Saitama, Japan.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Journal of medical virology</title><idno type="eISSN">1096-9071</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">Following the severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), another highly pathogenic coronavirus named SARS-CoV-2 (previously known as 2019-nCoV) emerged in December 2019 in Wuhan, China, and rapidly spreads around the world. This virus shares highly homological sequence with SARS-CoV, and causes acute, highly lethal pneumonia coronavirus disease 2019 (COVID-19) with clinical symptoms similar to those reported for SARS-CoV and MERS-CoV. The most characteristic symptom of patients with COVID-19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously. Additionally, some patients with COVID-19 also showed neurologic signs, such as headache, nausea, and vomiting. Increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the central nervous system inducing neurological diseases. The infection of SARS-CoV has been reported in the brains from both patients and experimental animals, where the brainstem was heavily infected. Furthermore, some coronaviruses have been demonstrated able to spread via a synapse-connected route to the medullary cardiorespiratory center from the mechanoreceptors and chemoreceptors in the lung and lower respiratory airways. Considering the high similarity between SARS-CoV and SARS-CoV2, it remains to make clear whether the potential invasion of SARS-CoV2 is partially responsible for the acute respiratory failure of patients with COVID-19. Awareness of this may have a guiding significance for the prevention and treatment of the SARS-CoV-2-induced respiratory failure.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">32104915</PMID><DateRevised><Year>2020</Year><Month>03</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-9071</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2020</Year><Month>Feb</Month><Day>27</Day></PubDate></JournalIssue><Title>Journal of medical virology</Title><ISOAbbreviation>J. Med. Virol.</ISOAbbreviation></Journal><ArticleTitle>The neuroinvasive potential of SARS-CoV2 may play a role in the respiratory failure of COVID-19 patients.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1002/jmv.25728</ELocationID><Abstract><AbstractText>Following the severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), another highly pathogenic coronavirus named SARS-CoV-2 (previously known as 2019-nCoV) emerged in December 2019 in Wuhan, China, and rapidly spreads around the world. This virus shares highly homological sequence with SARS-CoV, and causes acute, highly lethal pneumonia coronavirus disease 2019 (COVID-19) with clinical symptoms similar to those reported for SARS-CoV and MERS-CoV. The most characteristic symptom of patients with COVID-19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously. Additionally, some patients with COVID-19 also showed neurologic signs, such as headache, nausea, and vomiting. Increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the central nervous system inducing neurological diseases. The infection of SARS-CoV has been reported in the brains from both patients and experimental animals, where the brainstem was heavily infected. Furthermore, some coronaviruses have been demonstrated able to spread via a synapse-connected route to the medullary cardiorespiratory center from the mechanoreceptors and chemoreceptors in the lung and lower respiratory airways. Considering the high similarity between SARS-CoV and SARS-CoV2, it remains to make clear whether the potential invasion of SARS-CoV2 is partially responsible for the acute respiratory failure of patients with COVID-19. Awareness of this may have a guiding significance for the prevention and treatment of the SARS-CoV-2-induced respiratory failure.</AbstractText><CopyrightInformation>© 2020 Wiley Periodicals, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yan-Chao</ForeName><Initials>YC</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-2884-9829</Identifier><AffiliationInfo><Affiliation>Department of Histology and Embryology, College of Basic Medical Sciences, Norman Bethune College of Medicine, Jilin University, Changchun, Jilin, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bai</LastName><ForeName>Wan-Zhu</ForeName><Initials>WZ</Initials><AffiliationInfo><Affiliation>Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Science, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hashikawa</LastName><ForeName>Tsutomu</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Neural Architecture, Advanced Technology Development Group, RIKEN Brain Science Institute, Saitama, Japan.</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>02</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Med Virol</MedlineTA><NlmUniqueID>7705876</NlmUniqueID><ISSNLinking>0146-6615</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">cell susceptibility</Keyword><Keyword MajorTopicYN="N">coronavirus</Keyword><Keyword MajorTopicYN="N">dissemination</Keyword><Keyword MajorTopicYN="N">nervous system</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>02</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>02</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>2</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>2</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>2</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32104915</ArticleId><ArticleId IdType="doi">10.1002/jmv.25728</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Glass WG, Subbarao K, Murphy B, Murphy PM. 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