Influenza virus and SARS-CoV-2: pathogenesis and host responses in the respiratory tract.


Journal

Nature reviews. Microbiology
ISSN: 1740-1534
Titre abrégé: Nat Rev Microbiol
Pays: England
ID NLM: 101190261

Informations de publication

Date de publication:
07 2021
Historique:
accepted: 08 03 2021
pubmed: 8 4 2021
medline: 24 6 2021
entrez: 7 4 2021
Statut: ppublish

Résumé

Influenza viruses cause annual epidemics and occasional pandemics of respiratory tract infections that produce a wide spectrum of clinical disease severity in humans. The novel betacoronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in December 2019 and has since caused a pandemic. Both viral and host factors determine the extent and severity of virus-induced lung damage. The host's response to viral infection is necessary for viral clearance but may be deleterious and contribute to severe disease phenotypes. Similarly, tissue repair mechanisms are required for recovery from infection across the spectrum of disease severity; however, dysregulated repair responses may lead to chronic lung dysfunction. Understanding of the mechanisms of immunopathology and tissue repair following viral lower respiratory tract infection may broaden treatment options. In this Review, we discuss the pathogenesis, the contribution of the host response to severe clinical phenotypes and highlight early and late epithelial repair mechanisms following influenza virus infection, each of which has been well characterized. Although we are still learning about SARS-CoV-2 and its disease manifestations in humans, throughout the Review we discuss what is known about SARS-CoV-2 in the context of this broad knowledge of influenza virus, highlighting the similarities and differences between the respiratory viruses.

Identifiants

pubmed: 33824495
doi: 10.1038/s41579-021-00542-7
pii: 10.1038/s41579-021-00542-7
pmc: PMC8023351
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

425-441

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI154470
Pays : United States
Organisme : NIAID NIH HHS
ID : HHSN272201400006C
Pays : United States

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Auteurs

Tim Flerlage (T)

Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, USA.

David F Boyd (DF)

Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.

Victoria Meliopoulos (V)

Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, USA.

Paul G Thomas (PG)

Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA. paul.thomas@stjude.org.

Stacey Schultz-Cherry (S)

Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, USA. stacey.schultz-cherry@stjude.org.

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