ArticleJournal of virology2005
Human parainfluenza virus type 4 is incapable of evading the interferon-induced antiviral effect.
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 16 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.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Differential Induction and Signaling of Type I and III Interferons During Infection of Human Nasal Epithelial Cells With the Four Human Parainfluenza Virus Types.Journal of medical virology · 2026Article
- Distinct Evolutionary Signatures of Human Parainfluenza Viruses 2 and 4 Reveal Host Antagonism Divergence and Phylogenetic Discordance.Molecular biology and evolution · 2025Article
- Review
- Evasion of Host Antiviral Innate Immunity by Paramyxovirus Accessory Proteins.Frontiers in microbiology · 2021Review
- Evolutionary history of cotranscriptional editing in the paramyxoviral phosphoprotein gene.Virus evolution · 2021Review
- Tetherin antagonism by V proteins is a common trait among the genus Rubulavirus.Medical microbiology and immunology · 2017Article
- The Role of Human Parainfluenza Virus Infections in the Immunopathology of the Respiratory Tract.Current allergy and asthma reports · 2017Review
- La Piedad Michoacán Mexico Virus V protein antagonizes type I interferon response by binding STAT2 protein and preventing STATs nuclear translocation.Virus research · 2016Article
- Paramyxovirus evasion of innate immunity: Diverse strategies for common targets.World journal of virology · 2013Review
- The V protein of Tioman virus is incapable of blocking type I interferon signaling in human cells.PloS one · 2013Article
- Pathogenesis of acute respiratory illness caused by human parainfluenza viruses.Current opinion in virology · 2012Review
- Article
- Article
- Paramyxovirus disruption of interferon signal transduction: STATus report.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2009Review
- IFN-gamma regulation of ICAM-1 receptors in bronchial epithelial cells: soluble ICAM-1 release inhibits human rhinovirus infection.Journal of inflammation (London, England) · 2008Article
- Mapuera virus, a rubulavirus that inhibits interferon signalling in a wide variety of mammalian cells without degrading STATs.The Journal of general virology · 2007Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The V proteins of some paramyxoviruses have developed the ability to efficiently inactivate STAT protein function as a countermeasure for evading interferon (IFN) responses. Human parainfluenza virus type 4 (hPIV4) is one of the rubulaviruses, which are members of the family Paramyxoviridae, and has a V protein with a highly conserved cysteine-rich domain that is the hallmark of paramyxovirus V proteins. In order to study the function of the hPIV4 V protein, we established HeLa cells expressing the hPIV4A V protein (HeLa/FlagPIV4V). The hPIV4 V protein had no ability to reduce the level of STAT1 or STAT2, although it associated with STAT1, STAT2, DDB1, and Cul4A. It interfered with neither STAT1 and STAT2 tyrosine phosphorylation nor IFN-induced STAT nuclear accumulation. In addition, HeLa/FlagPIV4V cells are fully sensitive to both beta interferon (IFN-beta) and IFN-gamma, indicating that the hPIV4 V protein has no ability to block IFN-induced signaling. We further established HeLa cells expressing various chimeric proteins between the hPIV2 and hPIV4A V proteins. The lack of IFN-antagonistic activity of the hPIV4 V protein is caused by both the P/V common and V-specific domains. At least two regions (amino acids [aa] 32 to 45 and aa 143 to 164) of hPIV4 V in the P/V common domain and one region (aa 200 to 212) of the C terminus are involved in the inability to evade the IFN-induced signaling. Moreover, we established HeLa cells persistently infected with hPIV4 to make sure of the inability to escape IFN and confirmed that hPIV4 is the only paramyxovirus analyzed to date that can't evade the IFN-induced antiviral responses.
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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.