Innate immune responses to influenza A H5N1: friend or foe?
Open accessAbstract
Avian influenza A H5N1 remains unusual in its virulence for humans. Although infection of humans remains inefficient, many of those with H5N1 disease have a rapidly progressing viral pneumonia that leads to acute respiratory distress syndrome and death, but its pathogenesis remains an enigma. Comparison of the virology and pathogenesis of human seasonal influenza viruses (H3N2 and H1N1) and H5N1 in patients, animal models and relevant primary human cell cultures is instructive. Although the direct effects of viral replication and differences in the tropism of the virus for cells in the lower respiratory tract clearly contribute to pathogenesis, we focus here on the possible contribution of the host innate immune response in the pathogenesis of this disease.
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Influenza virus neuraminidase protein promotes adherence and invasion of S. pneumoniae through cleavage of sialic acid from the surfaces of host cells, thus exposing receptors for pneumococci.
“The influenza virus neuraminidase protein promotes adherence and invasion of S. pneumoniae through cleavage of sialic acid from the surfaces of host cells, thus exposing receptors for pneumococci (208).”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [208]
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- Authors
- Peiris, J. S. M., Cheung, C. Y., Leung, C. Y. H., & Nicholls, J. M.
- Affiliations
- Queen Mary Hospital (CN)
- University of Hong Kong (HK)
- Corresponding author
- Peiris, Joseph Sriyal Malik
- Venue
- Trends in Immunology
- Publisher
- Elsevier BV
- Published
- 2009-12
- Volume
- 30
- Issue
- 12
- Pages
- 574-584
- ISSN
- 1471-4906 (ISSN-L)
- PMC
- PMC5068224
- OpenAlex
- W2033321639
- Cited by
- 232
- References
- 99
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 6 · 2023: 9 · 2022: 13 · 2021: 14 · 2020: 29 · 2019: 6 · 2018: 16 · 2017: 12 · 2016: 10 · 2015: 14 · 2014: 18 · 2013: 22 · 2012: 15
- FWCI
- 2.12
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- The HKU Scholars Hub (University of Hong Kong) (submittedVersion)
- Funders
- University Grants Committee
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (HHSN266200700005C)
- Topics
- Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- H5N1 avian influenza, innate immune response, viral pathogenesis, acute respiratory distress syndrome, viral pneumonia, host-virus interaction, viral replication
- MeSH terms
- Animals, Humans, Immunity, Innate, Influenza, Human, Interferons, Orthomyxoviridae Infections, Respiratory Distress Syndrome, Tumor Necrosis Factor-alpha, Mice, Influenza A Virus, H1N1 Subtype, Influenza A Virus, H3N2 Subtype, Influenza A Virus, H5N1 Subtype
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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