ArticleJournal of virology2011
The viral nucleoprotein determines Mx sensitivity of influenza A viruses.
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 119 papers, 1 of them a synthesis that pooled it.
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Who cites it
119 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.
- Pooled it
- Influenza.Nature reviews. Disease primers · 2026Review
- In Vitro and Embryonic Evaluation of RecombinantPathogens (Basel, Switzerland) · 2026Article
- Independent proviral and antiviral host factors recognize the same capsid protein in divergent human herpesviruses.PLoS pathogens · 2026Article
- The potential of H5N1 viruses to adapt to bovine cells varies throughout evolution.Nature communications · 2025Article
- Genetic strategies for avian influenza resilience in poultry: from host-pathogen interaction studies to precision breeding.Functional & integrative genomics · 2025Review
- Human MX1 orchestrates the cytoplasmic sequestration of neosynthesized influenza A virus vRNPs.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Viral interferon antagonism shapes host tropism.PLoS pathogens · 2025Review
- Article
- Genetic resilience or resistance in poultry against avian influenza virus: mirage or reality?Journal of virology · 2025Review
- An ancient influenza genome from Switzerland allows deeper insights into host adaptation during the 1918 flu pandemic in Europe.BMC biology · 2025Article
- Heterozygous and generalist MxA super-restrictors overcome breadth-specificity trade-offs in antiviral restriction.Science advances · 2025Article
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
- Dissemination of influenza B virus to the lower respiratory tract of mice is restricted by the interferon response.Journal of virology · 2024Article
- Feasibility of Using a Type I IFN-Based Non-Animal Approach to Predict Vaccine Efficacy and Safety Profiles.Vaccines · 2024Review
- Bat-borne H9N2 influenza virus evades MxA restriction and exhibits efficient replication and transmission in ferrets.Nature communications · 2024Article
- The immune-evasive proline-283 substitution in influenza nucleoprotein increases aggregation propensity without altering the native structure.Science advances · 2024Article
- GTPase activity of porcine Mx1 plays a dominant role in inhibiting the N-Nsp9 interaction and thus inhibiting PRRSV replication.Journal of virology · 2024Article
- Influenza Virus Host Restriction Factors: The ISGs and Non-ISGs.Pathogens (Basel, Switzerland) · 2024Review
- Host factor MxA restricts Dabie bandavirus infection by targeting the viral NP protein to inhibit NP-RdRp interaction and ribonucleoprotein activity.Journal of virology · 2024Article
59 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
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host restriction factors play a crucial role in preventing trans-species transmission of viral pathogens. In mammals, the interferon-induced Mx GTPases are powerful antiviral proteins restricting orthomyxoviruses. Hence, the human MxA GTPase may function as an efficient barrier against zoonotic introduction of influenza A viruses into the human population. Successful viruses are likely to acquire adaptive mutations allowing them to evade MxA restriction. We compared the 2009 pandemic influenza A virus [strain A/Hamburg/4/09 (pH1N1)] with a highly pathogenic avian H5N1 isolate [strain A/Thailand/1(KAN-1)/04] for their relative sensitivities to human MxA and murine Mx1. The H5N1 virus was highly sensitive to both Mx GTPases, whereas the pandemic H1N1 virus was almost insensitive. Substitutions of the viral polymerase subunits or the nucleoprotein (NP) in a polymerase reconstitution assay demonstrated that NP was the main determinant of Mx sensitivity. The NP of H5N1 conferred Mx sensitivity to the pandemic H1N1 polymerase, whereas the NP of pandemic H1N1 rendered the H5N1 polymerase insensitive. Reassortant viruses which expressed the NP of H5N1 in a pH1N1 genetic background and vice versa were generated. Congenic Mx1-positive mice survived intranasal infection with these reassortants if the challenge virus contained the avian NP. In contrast, they succumbed to infection if the NP of pH1N1 origin was present. These findings clearly indicate that the origin of NP determines Mx sensitivity and that human influenza viruses acquired adaptive mutations to evade MxA restriction. This also explains our previous observations that human and avian influenza A viruses differ in their sensitivities to Mx.
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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.