ArticleVirology2013
Rift Valley fever virus NSs inhibits host transcription independently of the degradation of dsRNA-dependent protein kinase PKR.
Article in Virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- Cooperative role of PACT and ADAR1 in preventing aberrant PKR activation by self-derived double-stranded RNA.Nature communications · 2025Article
- Interactions of Equine Viruses with the Host Kinase Machinery and Implications for One Health and Human Disease.Viruses · 2023Review
- Article
- Harnessing Rift Valley fever virus NSs gene for cancer gene therapy.Cancer gene therapy · 2022Article
- NSG-Mice Reveal the Importance of a Functional Innate and Adaptive Immune Response to Overcome RVFV Infection.Viruses · 2022Article
- The Atypical Kinase RIOK3 Limits RVFV Propagation and Is Regulated by Alternative Splicing.Viruses · 2021Article
- Article
- Inhibition of PKR by Viruses.Frontiers in microbiology · 2021Review
- Rescue of infectious Arumowot virus from cloned cDNA: Posttranslational degradation of Arumowot virus NSs protein in human cells.PLoS neglected tropical diseases · 2019Article
- Combination Kinase Inhibitor Treatment Suppresses Rift Valley Fever Virus Replication.Viruses · 2018Article
- The Emergence of Severe Fever with Thrombocytopenia Syndrome Virus.The American journal of tropical medicine and hygiene · 2017Review
- Rapamycin modulation of p70 S6 kinase signaling inhibits Rift Valley fever virus pathogenesis.Antiviral research · 2017Article
- Rift Valley fever virus NSs protein functions and the similarity to other bunyavirus NSs proteins.Virology journal · 2016Review
- Mutational Analysis of the Rift Valley Fever Virus Glycoprotein Precursor Proteins for Gn Protein Expression.Viruses · 2016Article
- N-Glycans on the Rift Valley Fever Virus Envelope Glycoproteins Gn and Gc Redundantly Support Viral Infection via DC-SIGN.Viruses · 2016Article
- Protein Kinase R Degradation Is Essential for Rift Valley Fever Virus Infection and Is Regulated by SKP1-CUL1-F-box (SCF)FBXW11-NSs E3 Ligase.PLoS pathogens · 2016Article
- Cytokine response in mouse bone marrow derived macrophages after infection with pathogenic and non-pathogenic Rift Valley fever virus.The Journal of general virology · 2015Article
- Interplay between the Virus and Host in Rift Valley Fever Pathogenesis.Journal of innate immunity · 2015Article
- The consequences of reconfiguring the ambisense S genome segment of Rift Valley fever virus on viral replication in mammalian and mosquito cells and for genome packaging.PLoS pathogens · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Rift Valley fever virus (RVFV) encodes one major virulence factor, the NSs protein. NSs suppresses host general transcription, including interferon (IFN)-β mRNA synthesis, and promotes degradation of the dsRNA-dependent protein kinase (PKR). We generated a novel RVFV mutant (rMP12-NSsR173A) specifically lacking the function to promote PKR degradation. rMP12-NSsR173A infection induces early phosphorylation of eIF2α through PKR activation, while retaining the function to inhibit host general transcription including IFN-β gene inhibition. MP-12 NSs but not R173A NSs binds to wt PKR. R173A NSs formed filamentous structure in nucleus in a mosaic pattern, which was distinct from MP-12 NSs filament pattern. Due to early phosphorylation of eIF2α, rMP12-NSsR173A could not efficiently accumulate viral proteins. Our results suggest that NSs-mediated host general transcription suppression occurs independently of PKR degradation, while the PKR degradation is important to inhibit the phosphorylation of eIF2α in infected cells undergoing host general transcription suppression.
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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.