ReviewCold Spring Harbor perspectives in medicine2021
Host Cell Factors That Interact with Influenza Virus Ribonucleoproteins.
Review in Cold Spring Harbor perspectives in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Breaking barriers: Respiratory viral strategies targeting the host's nuclear pore complex and nuclear transport pathways.Molecular biology of the cell · 2026Review
- The viral proteins of influenza A virus competitively bind to TRIM31 with MAVS to fine-tune the antiviral innate immunity.Journal of virology · 2025Article
- Nanchangmycin suppresses influenza A virus infection by blocking endosomal acidification.Acta biochimica et biophysica Sinica · 2025Article
- Screening of neurotransmitter receptor modulators reveals novel inhibitors of influenza virus replication.Frontiers in cellular and infection microbiology · 2025Article
- hnRNPH1 Inhibits Influenza Virus Replication by Binding Viral RNA.Microorganisms · 2024Article
- The RBPome of influenza A virus NP-mRNA reveals a role for TDP-43 in viral replication.Nucleic acids research · 2024Article
- Unravelling the interaction between Influenza virus and the nuclear pore complex: insights into viral replication and host immune response.Virusdisease · 2024Review
- The Identification Distinct Antiviral Factors Regulated Influenza Pandemic H1N1 Infection.International journal of microbiology · 2024Article
- Evaluation of the Antiviral Activity of Tabamide A and Its Structural Derivatives against Influenza Virus.International journal of molecular sciences · 2023Article
- Pathogenicity and virulence of influenza.Virulence · 2023Review
- Defining the minimal components of the influenza A virus replication machinery via an in vitro reconstitution system.PLoS biology · 2023Article
- An Influenza A virus can evolve to use human ANP32E through altering polymerase dimerization.Nature communications · 2023Article
- Avian Influenza Virus Tropism in Humans.Viruses · 2023Review
- Upregulation of galectin-3 in influenza A virus infection promotes viral RNA synthesis through its association with viral PA protein.Journal of biomedical science · 2023Article
- The C-terminal LCAR of host ANP32 proteins interacts with the influenza A virus nucleoprotein to promote the replication of the viral RNA genome.Nucleic acids research · 2022Article
- KPNA6 is a Cofactor of ANP32A/B in Supporting Influenza Virus Polymerase Activity.Microbiology spectrum · 2022Article
- A natural variant in ANP32B impairs influenza virus replication in human cells.The Journal of general virology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Influenza viruses hijack host cell factors at each stage of the viral life cycle. After host cell entry and endosomal escape, the influenza viral ribonucleoproteins (vRNPs) are released into the cytoplasm where the classical cellular nuclear import pathway is usurped for nuclear translocation of the vRNPs. Transcription takes place inside the nucleus at active host transcription sites, and cellular mRNA export pathways are subverted for export of viral mRNAs. Newly synthesized RNP components cycle back into the nucleus using various cellular nuclear import pathways and host-encoded chaperones. Replication of the negative-sense viral RNA (vRNA) into complementary RNA (cRNA) and back into vRNA requires complex interplay between viral and host factors. Progeny vRNPs assemble at the host chromatin and subsequently exit from the nucleus-processes orchestrated by sets of host and viral proteins. Finally, several host pathways appear to play a role in vRNP trafficking from the nuclear envelope to the plasma membrane for egress.
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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.