ArticleNature communications2012
Adaptive mutations in NEP compensate for defective H5N1 RNA replication in cultured human cells.
Article in Nature communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 145 citations in OpenAlex.
- Regulatory hotspot on the influenza A virus polymerase revealed through the structure of the NEP-polymerase complex.Science advances · 2026Article
- Polymerase mutations underlie early adaptation of H5N1 influenza virus to dairy cattle and other mammals.Nature communications · 2026Article
- Analysis of NS2-dependent effects on influenza PB1 segment extends replication requirements beyond the canonical promoter.Nature communications · 2025Article
- Probing the functional constraints of influenza A virus NEP by deep mutational scanning.Cell reports · 2025Article
- Influenza A virus NS2 protein acts on vRNA-resident polymerase to drive the transcription to replication switch.Nucleic acids research · 2025Article
- Human ANP32A/B are SUMOylated and utilized by avian influenza virus NS2 protein to overcome species-specific restriction.Nature communications · 2024Article
- Structures of influenza A and B replication complexes give insight into avian to human host adaptation and reveal a role of ANP32 as an electrostatic chaperone for the apo-polymerase.Nature communications · 2024Article
- OTUB1 contributes to the stability and function of Influenza A virus NS2.PLoS pathogens · 2024Article
- Unveiling the role of host kinases at different steps of influenza A virus life cycle.Journal of virology · 2024Review
- Twenty natural amino acid substitution screening at the last residue 121 of influenza A virus NS2 protein reveals the critical role of NS2 in promoting virus genome replication by coordinating with viral polymerase.Journal of virology · 2024Article
- Creating resistance to avian influenza infection through genome editing of the ANP32 gene family.Nature communications · 2023Article
- Fitness Determinants of Influenza A Viruses.Viruses · 2023Review
- Influenza virus transcription and progeny production are poorly correlated in single cells.eLife · 2023Article
- Continued Circulation of Highly Pathogenic H5 Influenza Viruses in Vietnamese Live Bird Markets in 2018-2021.Viruses · 2023Article
- The SUMO-interacting motif in NS2 promotes adaptation of avian influenza virus to mammals.Science advances · 2023Article
- Fine Regulation of Influenza Virus RNA Transcription and Replication by Stoichiometric Changes in Viral NS1 and NS2 Proteins.Journal of virology · 2023Article
- Article
- The ubiquitination landscape of the influenza A virus polymerase.Nature communications · 2023Article
- NS2 is a key determinant of compatibility in reassortant avian influenza virus with heterologous H7N9-derived NS segment.Virus research · 2023Article
- Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection of mammals by avian influenza viruses requires adaptive mutations to achieve high-level replication in the new host. However, the basic mechanism underlying this adaptation process is still unknown. Here we show that avian polymerases, lacking the human signature PB2-E627K, are incapable of generating usable complementary RNA templates in cultured human cells and therefore require adaptation. Characterization of the highly pathogenic human H5N1 isolate A/Thailand/1(KAN-1)/2004 that retained the avian PB2-E627 reveals that the defect in RNA replication is only partially compensated by mutations in the polymerase. Instead, mutations in the nuclear export protein are required for efficient polymerase activity. We demonstrate that adaptive mutations in nuclear export proteins of several human isolates enhance the polymerase activity of avian polymerases in human cultured cells. In conclusion, when crossing the species barrier, avian influenza viruses acquire adaptive mutations in nuclear export protein to escape restricted viral genome replication in mammalian cells.
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