Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology.
Identifieur interne : 000C98 ( PubMed/Corpus ); précédent : 000C97; suivant : 000C99Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology.
Auteurs : Rudragouda Channappanavar ; Stanley PerlmanSource :
- Seminars in immunopathology [ 1863-2300 ] ; 2017.
English descriptors
- KwdEn :
- Animals, Antiviral Agents (pharmacology), Chemokines (metabolism), Combined Modality Therapy, Coronavirus (drug effects), Coronavirus (physiology), Coronavirus Infections (diagnosis), Coronavirus Infections (immunology), Coronavirus Infections (metabolism), Coronavirus Infections (virology), Cytokines (metabolism), Disease Models, Animal, Disease Susceptibility, Humans, Immune System (cytology), Immune System (immunology), Immune System (metabolism), Immunity, Innate, Interferons (metabolism), Interferons (pharmacology), Lung (immunology), Lung (metabolism), Lung (pathology), Lung (virology), Macrophages (immunology), Monocytes (immunology), Monocytes (metabolism), Phenotype, Severity of Illness Index, Virus Replication (drug effects), Virus Replication (immunology).
- MESH :
- chemical , metabolism : Chemokines, Cytokines, Interferons.
- chemical , pharmacology : Antiviral Agents, Interferons.
- cytology : Immune System.
- diagnosis : Coronavirus Infections.
- drug effects : Coronavirus, Virus Replication.
- immunology : Coronavirus Infections, Immune System, Lung, Macrophages, Monocytes, Virus Replication.
- metabolism : Coronavirus Infections, Immune System, Lung, Monocytes.
- pathology : Lung.
- physiology : Coronavirus.
- virology : Coronavirus Infections, Lung.
- Animals, Combined Modality Therapy, Disease Models, Animal, Disease Susceptibility, Humans, Immunity, Innate, Phenotype, Severity of Illness Index.
Abstract
Human coronaviruses (hCoVs) can be divided into low pathogenic and highly pathogenic coronaviruses. The low pathogenic CoVs infect the upper respiratory tract and cause mild, cold-like respiratory illness. In contrast, highly pathogenic hCoVs such as severe acute respiratory syndrome CoV (SARS-CoV) and Middle East respiratory syndrome CoV (MERS-CoV) predominantly infect lower airways and cause fatal pneumonia. Severe pneumonia caused by pathogenic hCoVs is often associated with rapid virus replication, massive inflammatory cell infiltration and elevated pro-inflammatory cytokine/chemokine responses resulting in acute lung injury (ALI), and acute respiratory distress syndrome (ARDS). Recent studies in experimentally infected animal strongly suggest a crucial role for virus-induced immunopathological events in causing fatal pneumonia after hCoV infections. Here we review the current understanding of how a dysregulated immune response may cause lung immunopathology leading to deleterious clinical manifestations after pathogenic hCoV infections.
DOI: 10.1007/s00281-017-0629-x
PubMed: 28466096
Links to Exploration step
pubmed:28466096Le document en format XML
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The low pathogenic CoVs infect the upper respiratory tract and cause mild, cold-like respiratory illness. In contrast, highly pathogenic hCoVs such as severe acute respiratory syndrome CoV (SARS-CoV) and Middle East respiratory syndrome CoV (MERS-CoV) predominantly infect lower airways and cause fatal pneumonia. Severe pneumonia caused by pathogenic hCoVs is often associated with rapid virus replication, massive inflammatory cell infiltration and elevated pro-inflammatory cytokine/chemokine responses resulting in acute lung injury (ALI), and acute respiratory distress syndrome (ARDS). Recent studies in experimentally infected animal strongly suggest a crucial role for virus-induced immunopathological events in causing fatal pneumonia after hCoV infections. Here we review the current understanding of how a dysregulated immune response may cause lung immunopathology leading to deleterious clinical manifestations after pathogenic hCoV infections.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28466096</PMID><DateCompleted><Year>2018</Year><Month>03</Month><Day>26</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1863-2300</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>5</Issue><PubDate><Year>2017</Year><Month>07</Month></PubDate></JournalIssue><Title>Seminars in immunopathology</Title><ISOAbbreviation>Semin Immunopathol</ISOAbbreviation></Journal><ArticleTitle>Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology.</ArticleTitle><Pagination><MedlinePgn>529-539</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00281-017-0629-x</ELocationID><Abstract><AbstractText>Human coronaviruses (hCoVs) can be divided into low pathogenic and highly pathogenic coronaviruses. The low pathogenic CoVs infect the upper respiratory tract and cause mild, cold-like respiratory illness. In contrast, highly pathogenic hCoVs such as severe acute respiratory syndrome CoV (SARS-CoV) and Middle East respiratory syndrome CoV (MERS-CoV) predominantly infect lower airways and cause fatal pneumonia. Severe pneumonia caused by pathogenic hCoVs is often associated with rapid virus replication, massive inflammatory cell infiltration and elevated pro-inflammatory cytokine/chemokine responses resulting in acute lung injury (ALI), and acute respiratory distress syndrome (ARDS). Recent studies in experimentally infected animal strongly suggest a crucial role for virus-induced immunopathological events in causing fatal pneumonia after hCoV infections. Here we review the current understanding of how a dysregulated immune response may cause lung immunopathology leading to deleterious clinical manifestations after pathogenic hCoV infections.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Channappanavar</LastName><ForeName>Rudragouda</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Microbiology, University of Iowa, BSB 3-712, Iowa City, IA, 52242, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perlman</LastName><ForeName>Stanley</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Microbiology, University of Iowa, BSB 3-712, Iowa City, IA, 52242, USA. 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