ArticleVirology2016
Functional motifs responsible for human metapneumovirus M2-2-mediated innate immune evasion.
Article in Virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- Review
- Mechanistic insights and emerging applications of human metapneumovirus (HMPV) treatment: From molecular design to translational immunity.Folia microbiologica · 2026Review
- Human metapneumovirus: pathogenesis, epidemiology, diagnostic technologies, and potential intervention strategies.Virology journal · 2025Review
- Human metapneumovirus: understanding the molecular mechanisms and pathology of infection.Journal of virology · 2025Review
- Review
- The role of M2 proteins of pneumoviruses in transcription regulation, prevention of hypermutation, and activation of the type I interferon pathway.Journal of virology · 2025Article
- Evidence against the Human Metapneumovirus G, SH, and M2-2 Proteins as Bona Fide Interferon Antagonists.Journal of virology · 2022Article
- Regulation of antiviral innate immune signaling and viral evasion following viral genome sensing.Experimental & molecular medicine · 2021Review
- Substituted N-(4-amino-2-chlorophenyl)-5-chloro-2-hydroxybenzamide analogues potently inhibit respiratory syncytial virus (RSV) replication and RSV infection-associated inflammatory responses.Bioorganic & medicinal chemistry · 2021Article
- The role of M2-2 PDZ-binding motifs in pulmonary innate immune responses to human metapneumovirus.Journal of medical virology · 2020Article
- Regulation of MAVS Expression and Signaling Function in the Antiviral Innate Immune Response.Frontiers in immunology · 2020Review
- Human Type I Interferon Antiviral Effects in Respiratory and Reemerging Viral Infections.Journal of immunology research · 2020Review
- Prophylactic and therapeutic approaches for human metapneumovirus.Virusdisease · 2018Review
- Exchange Proteins Directly Activated by cAMP and Their Roles in Respiratory Syncytial Virus Infection.Journal of virology · 2018Article
- Review
- Review
- Article
- Human Metapneumovirus: Mechanisms and Molecular Targets Used by the Virus to Avoid the Immune System.Frontiers in immunology · 2018Review
- Detection of Nuclear Protein Profile Changes by Human Metapneumovirus M2-2 Protein Using Quantitative Differential Proteomics.Vaccines · 2017Article
- Human Metapneumovirus M2-2 Protein Acts as a Negative Regulator of Alpha Interferon Production by Plasmacytoid Dendritic Cells.Journal of virology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Human metapneumovirus (hMPV) is a major cause of lower respiratory infection in young children. Repeated infections occur throughout life, but its immune evasion mechanisms are largely unknown. We recently found that hMPV M2-2 protein elicits immune evasion by targeting mitochondrial antiviral-signaling protein (MAVS), an antiviral signaling molecule. However, the molecular mechanisms underlying such inhibition are not known. Our mutagenesis studies revealed that PDZ-binding motifs, 29-DEMI-32 and 39-KEALSDGI-46, located in an immune inhibitory region of M2-2, are responsible for M2-2-mediated immune evasion. We also found both motifs prevent TRAF5 and TRAF6, the MAVS downstream adaptors, to be recruited to MAVS, while the motif 39-KEALSDGI-46 also blocks TRAF3 migrating to MAVS. In parallel, these TRAFs are important in activating transcription factors NF-kB and/or IRF-3 by hMPV. Our findings collectively demonstrate that M2-2 uses its PDZ motifs to launch the hMPV immune evasion through blocking the interaction of MAVS and its downstream TRAFs.
Indexed as
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What OpenQuestion holds
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.