ArticleJournal of virology2010
MyD88 signaling is indispensable for primary influenza A virus infection but dispensable for secondary infection.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
65 citing papers in PubMed, 94 citations in OpenAlex.
- Primordial germ cell-derived macrophages as a platform to study host-pathogen interactions.Frontiers in cell and developmental biology · 2026Article
- SARS-CoV-2 infection primes cross-protective respiratory IgA in a MyD88- and MAVS-dependent manner.NPJ vaccines · 2025Article
- The E3 ligase ASB3 downregulates antiviral innate immunity by targeting MAVS for ubiquitin-proteasomal degradation.Cell death and differentiation · 2024Article
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
- Sex-related immunity: could Toll-like receptors be the answer in acute inflammatory response?Frontiers in immunology · 2024Review
- Comparison of media for a human peripheral blood mononuclear cell-basedClinical and experimental vaccine research · 2023Article
- Formulation, inflammation, and RNA sensing impact the immunogenicity of self-amplifying RNA vaccines.Molecular therapy. Nucleic acids · 2023Article
- Neutrophil subsets and their differential roles in viral respiratory diseases.Journal of leukocyte biology · 2022Review
- Type I interferons and MAVS signaling are necessary for tissue resident memory CD8+ T cell responses to RSV infection.PLoS pathogens · 2022Article
- Screening of Antiviral Components of Yinhuapinggan Granule and Protective Effects of Yinhuapinggan Granule on MDCK Cells with Influenza A/H1N1 Virus.BioMed research international · 2022Article
- Prospects on Repurposing a Live Attenuated Vaccine for the Control of Unrelated Infections.Frontiers in immunology · 2022Review
- Article
- Neutrophils in respiratory viral infections.Mucosal immunology · 2021Review
- Review
- Targeting TLR4 Signaling to Blunt Viral-Mediated Acute Lung Injury.Frontiers in immunology · 2021Review
- Review
- Complex Genetic Architecture Underlies Regulation of Influenza-A-Virus-Specific Antibody Responses in the Collaborative Cross.Cell reports · 2020Article
- Review
- Paradoxical modulation of influenza by intranasal administration of non-replicating adenovirus particles.PloS one · 2020Article
- Pattern Recognition Receptor Signaling and Innate Responses to Influenza A Viruses in the Mallard Duck, Compared to Humans and Chickens.Frontiers in cellular and infection microbiology · 2020Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have revealed that innate immunity is involved in the development of adaptive immune responses; however, its role in protection is not clear. In order to elucidate the exact role of Toll-like receptor (TLR) or RIG-I-like receptor (RLR) signaling on immunogenicity and protective efficacy against influenza A virus infection (A/PR/8/34 [PR8]; H1N1), we adapted several innate signal-deficient mice (e.g., TRIF(-/-), MyD88(-/-), MyD88(-/-) TRIF(-/-), TLR3(-/-) TLR7(-/-), and IPS-1(-/-)). In this study, we found that MyD88 signaling was required for recruitment of CD11b(+) granulocytes, production of early inflammatory cytokines, optimal proliferation of CD4 T cells, and production of Th1 cytokines by T cells. However, PR8 virus-specific IgG and IgA antibody levels in both systemic and mucosal compartments were normal in TLR- and RLR-deficient mice. To further assess the susceptibility of these mice to influenza virus infection, protective efficacy was determined after primary or secondary lethal challenge. We found that MyD88(-/-) and MyD88(-/-) TRIF(-/-) mice were more susceptible to primary influenza virus infection than the B6 mice but were fully protected against homologous (H1N1) and heterosubtypic (H5N2) secondary infection when primed with a nonlethal dose of PR8 virus. Taken together, these results show that MyD88 signaling plays an important role for resisting primary influenza virus infection but is dispensable for protection against a secondary lethal challenge.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.