ArticleJournal of virology2011
The cellular RNA helicase UAP56 is required for prevention of double-stranded RNA formation during influenza A virus infection.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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53 citing papers in PubMed, 73 citations in OpenAlex.
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- Influenza A virus circumvents the innate immune response through the sequestration of double-stranded RNA.Journal of virology · 2025Article
- Genetic resilience or resistance in poultry against avian influenza virus: mirage or reality?Journal of virology · 2025Review
- Defining the balance between optimal immunity and immunopathology in influenza virus infection.Nature reviews. Immunology · 2024Review
- Critical Cellular Functions and Mechanisms of Action of the RNA Helicase UAP56.Journal of molecular biology · 2024Review
- Structural basis for high-order complex of SARNP and DDX39B to facilitate mRNP assembly.Cell reports · 2023Article
- Influenza A virus NS1 protein hijacks YAP/TAZ to suppress TLR3-mediated innate immune response.PLoS pathogens · 2022Article
- De Novo Assembly of 20 Chicken Genomes Reveals the Undetectable Phenomenon for Thousands of Core Genes on Microchromosomes and Subtelomeric Regions.Molecular biology and evolution · 2022Article
- Host Cell Factors That Interact with Influenza Virus Ribonucleoproteins.Cold Spring Harbor perspectives in medicine · 2021Review
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- Precision Vaccine Development: Cues From Natural Immunity.Frontiers in immunology · 2021Review
- Molecular Evolution of the Influenza A Virus Non-structural Protein 1 in Interspecies Transmission and Adaptation.Frontiers in microbiology · 2021Review
- Innate Immune Sensing of Influenza A Virus.Viruses · 2020Review
- Mx genes: host determinants controlling influenza virus infection and trans-species transmission.Human genetics · 2020Review
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- Chemical intervention of influenza virus mRNA nuclear export.PLoS pathogens · 2020Article
- DDX39B interacts with the pattern recognition receptor pathway to inhibit NF-κB and sensitize to alkylating chemotherapy.BMC biology · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cellular DEAD box RNA helicase UAP56 plays a pivotal role in the efficient transcription/replication of influenza A virus. UAP56 is recruited by the nucleoprotein (NP) of influenza A viruses, and recent data revealed that the RNA helicase is required for the nuclear export of a subset of spliced and unspliced viral mRNAs. The fact that influenza viruses do not produce detectable amounts of double-stranded RNA (dsRNA) intermediates during transcription/replication suggests the involvement of cellular RNA helicases. Hence, we examined whether the RNA-unwinding activity of UAP56 or its paralog URH49 plays a role in preventing the accumulation of dsRNA during infection. First, our data showed that not only UAP56 but also its paralog URH49 can interact with NPs of avian and human influenza A viruses. The small interfering RNA (siRNA)-mediated depletion of either RNA helicase reduced the transport of M1 and hemagglutinin (HA) mRNAs and, to a lesser extent, NP and NS1 mRNAs into the cytoplasm. Moreover, we found that virus infection of UAP56-depleted cells leads to the rapid accumulation of dsRNA in the perinuclear region. In parallel, we observed a robust virus-mediated activation of dsRNA-dependent protein kinase R (PKR), indicating that the cellular RNA helicase UAP56 may be recruited by influenza virus to prevent dsRNA formation. The accumulation of dsRNA was blocked when actinomycin D or cycloheximide was used to inhibit viral transcription/replication or translation, respectively. In summary, we demonstrate that UAP56 is utilized by influenza A viruses to prevent the formation of dsRNA and, hence, the activation of the innate immune response.
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