ArticleJournal of virology2005
Overexpression of the M2-2 protein of respiratory syncytial virus inhibits viral replication.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 55 citations in OpenAlex.
- Article
- RSV vaccine development: advances and fusion protein-focused strategies.Frontiers in immunology · 2026Review
- Human metapneumovirus: understanding the molecular mechanisms and pathology of infection.Journal of virology · 2025Review
- 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
- Expression and Purification of Recombinant Respiratory Syncytial Virus Proteins.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Identification of distinct genotypes in circulating RSV A strains based on variants in the virus replication-associated genes.Journal of virology · 2024Article
- Identification of distinct genotypes in circulating RSV A strains based on variants on the virus replication-associated genes.bioRxiv : the preprint server for biology · 2024Article
- Respiratory Syncytial Virus: A Comprehensive Review of Transmission, Pathophysiology, and Manifestation.Cureus · 2023Review
- Rescue of codon-pair deoptimized respiratory syncytial virus by the emergence of genomes with very large internal deletions that complemented replication.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Polymerase-tagged respiratory syncytial virus reveals a dynamic rearrangement of the ribonucleocapsid complex during infection.PLoS pathogens · 2020Article
- Modulation of Host Immunity by Human Respiratory Syncytial Virus Virulence Factors: A Synergic Inhibition of Both Innate and Adaptive Immunity.Frontiers in cellular and infection microbiology · 2017Review
- Human Respiratory Syncytial Virus: Infection and Pathology.Seminars in respiratory and critical care medicine · 2016Review
- Functional correlations of respiratory syncytial virus proteins to intrinsic disorder.Molecular bioSystems · 2016Article
- Review
- Structural analysis of respiratory syncytial virus reveals the position of M2-1 between the matrix protein and the ribonucleoprotein complex.Journal of virology · 2014Article
- Modulation of host adaptive immunity by hRSV proteins.Virulence · 2014Review
- The comparative genomics of human respiratory syncytial virus subgroups A and B: genetic variability and molecular evolutionary dynamics.Journal of virology · 2013Article
- Respiratory syncytial virus: virology, reverse genetics, and pathogenesis of disease.Current topics in microbiology and immunology · 2013Article
- Emerging roles for the influenza A virus nuclear export protein (NEP).PLoS pathogens · 2012Review
- Whole genome characterization of non-tissue culture adapted HRSV strains in severely infected children.Virology journal · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The M2-2 protein of respiratory syncytial virus (RSV) is involved in regulation of viral RNA transcription and replication. Encoded by the next-to-last gene of RSV, the M2-2 open reading frame (ORF) overlaps with the upstream M2-1 ORF, suggesting that the production of the M2-2 protein might be tightly regulated during virus replication. To evaluate the effect of M2-2 overexpression on RSV replication, the M2-2 gene was separated from M2-1 by leaving it at the position prior to the M2-1 or moving it to the promoter proximal position as an independent transcriptional unit in the RSV A2 genome. Although recombinant viruses bearing the shuffled M2-2 gene were recovered and expressed higher levels of M2-2, most of these viruses grew poorly in HEp-2 cells. Sequence analysis revealed that various mutations (substitution, insertion, and deletion) occurred in the M2-2 gene, resulting in reduced M2-2 activity as measured by the RSV minigenome system. Further examination of the M2-2 sequence and its function showed that either one of the first two AUG codons located at the 5' end of M2-2 could be used to produce a functional M2-2 protein and that deletion of the first six amino acids from its N terminus or four amino acids from its C terminus greatly reduced its function. The effect of M2-2 protein on RSV replication was also studied by examining RSV replication in cells transiently expressing M2-2. The M2-2 protein expressed at a high level completely inhibited RSV replication. These results strongly suggested that the level of the M2-2 protein produced in the infected cells is critical to RSV replication.
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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.