ArticleInflammation2013
MHV68 latency modulates the host immune response to influenza A virus.
Article in Inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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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
16 citing papers in PubMed, 30 citations in OpenAlex.
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- Prior infection with unrelated neurotropic virus exacerbates influenza disease and impairs lung T cell responses.Nature communications · 2024Article
- Review
- Cross-Reactive T Cell Response Exists in Chronic Lymphocytic Choriomeningitis Virus Infection upon Pichinde Virus Challenge.Viruses · 2022Article
- Qing-Wen-Jie-Re Mixture Ameliorates Poly (I:C)-Induced Viral Pneumonia Through Regulating the Inflammatory Response and Serum Metabolism.Frontiers in pharmacology · 2022Article
- Prospects on Repurposing a Live Attenuated Vaccine for the Control of Unrelated Infections.Frontiers in immunology · 2022Review
- Conquering the Host: Determinants of Pathogenesis Learned from Murine Gammaherpesvirus 68.Annual review of virology · 2021Article
- A gammaherpesvirus licenses CD8 T cells to protect the host from pneumovirus-induced immunopathologies.Mucosal immunology · 2020Article
- The effect of respiratory viruses on immunogenicity and protection induced by a candidate universal influenza vaccine in mice.PloS one · 2019Article
- Past Life and Future Effects-How Heterologous Infections Alter Immunity to Influenza Viruses.Frontiers in immunology · 2018Review
- Susceptibility of bone marrow-derived macrophages to influenza virus infection is dependent on macrophage phenotype.The Journal of general virology · 2015Article
- Article
- Helminth infection reactivates latent γ-herpesvirus via cytokine competition at a viral promoter.Science (New York, N.Y.) · 2014Article
- Toxoplasma gondii profilin promotes recruitment of Ly6Chi CCR2+ inflammatory monocytes that can confer resistance to bacterial infection.PLoS pathogens · 2014Article
- Kingdom-agnostic metagenomics and the importance of complete characterization of enteric microbial communities.Gastroenterology · 2014Review
- Latent gammaherpesvirus 68 infection induces distinct transcriptional changes in different organs.Journal of virology · 2014Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Murine gammaherpesvirus 68 (MHV68) is a natural rodent pathogen that has been used as a model to study the pathogenesis of human gammaherpesviruses. Like other herpesviruses, MHV68 causes acute infection and establishes life-long latency in the host. Recently, it has been shown that mice latently infected with MHV68 have resistance to unrelated pathogens in secondary infection models. We therefore hypothesized that latent MHV68 infection could modulate the host response to influenza A virus. To test this hypothesis, mice were infected intranasally with influenza virus following the establishment of MHV68 latency. Mice latently infected with MHV68 showed significantly higher survival to influenza A virus infection than did PBS mock-infected mice. Latent MHV68 infection led to lower influenza viral loads and decreased inflammatory pathology in the lungs. Alveolar macrophages of mice latently infected with MHV68 showed activated status, and adoptive transfer of those activated macrophages into mice followed the infection with influenza A virus had significantly greater survival rates than control mice, suggesting that activated alveolar macrophages are a key mechanistic component in protection from secondary infections.
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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.