Evidence map›Paper›PMID 23015697›Full record

ArticleJournal of virology2012

Human metapneumovirus M2-2 protein inhibits innate cellular signaling by targeting MAVS.

Junping Ren, Qingrong Wang, Deepthi Kolli, Deborah J Prusak, Chien-Te K Tseng, Zhijian J Chen, Kui Li, Thomas G Wood, Xiaoyong Bao

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 65 citations in OpenAlex.

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  13. Receptors and host factors: key players in human metapneumovirus infection.Frontiers in cellular and infection microbiology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Junping RenDepartment of Pediatrics, University of Texas Medical Branch, Galveston, Texas, USA.
Qingrong Wang
Deepthi Kolli
Deborah J Prusak
Chien-Te K Tseng
Zhijian J Chen
Kui Li
Thomas G Wood
Xiaoyong Bao
The University of Texas Medical Branch at Galveston · USHoward Hughes Medical Institute · USUniversity of Tennessee Health Science Center · US

Funding

Cellular responses to human metapneumovirus infectionK22AI074829 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI BAO, XIAOYONG · 2010 to 2011
$270k
Howard Hughes Medical InstituteNIAID NIH HHS K22 AI074829PHS HHS KAI074829A
6 · The paper itself

Abstract

Human metapneumovirus (hMPV) is a leading cause of respiratory infections in pediatric populations globally, with no prophylactic or therapeutic measures. Recently, a recombinant hMPV lacking the M2-2 protein (rhMPV-ΔM2-2) demonstrated reduced replication in the respiratory tract of animal models, making it a promising live vaccine candidate. However, the exact nature of the interaction between the M2-2 protein and host cells that regulates viral infection/propagation is largely unknown. By taking advantage of the available reverse genetics system and ectopic expression system for viral protein, we found that M2-2 not only promotes viral gene transcription and replication but subverts host innate immunity, therefore identifying M2-2 as a novel virulence factor, in addition to the previously described hMPV G protein. Since we have shown that the RIG-I/MAVS pathway plays an important role in hMPV-induced signaling in airway epithelial cells, we investigated whether M2-2 antagonizes the host cellular responses by targeting this pathway. Reporter gene assays and coimmunoprecipitation studies indicated that M2-2 targets MAVS, an inhibitory mechanism different from what we previously reported for hMPV G, which affects RIG-I- but not MAVS-dependent gene transcription. In addition, we found that the domains of M2-2 responsible for the regulation of viral gene transcription and antiviral signaling are different. Our findings collectively demonstrate that M2-2 contributes to hMPV immune evasion through the inhibition of MAVS-dependent cellular responses.

Indexed as

Adaptor Proteins, Signal TransducingAnalysis of VarianceAnimalsBlotting, WesternChlorocebus aethiopsDNA PrimersHumansImmune EvasionImmunoprecipitationMetapneumovirusPlasmidsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionSignal TransductionTranscription, GeneticVero CellsAdaptor Proteins, Signal TransducingDNA PrimersMAVS protein, humanViral ProteinsVirulence Factors

Identifiers

PMID23015697
PMCPMC3497653
OpenAlexW2166681612

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.