ArticleJournal of virology2013
1918 Influenza virus hemagglutinin (HA) and the viral RNA polymerase complex enhance viral pathogenicity, but only HA induces aberrant host responses in mice.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Historical Pandemic and Contemporary Influenza A Viruses Reveal PB2 M631L as a Convergent Adaptation to Human ANP32.Microorganisms · 2026Article
- An ancient influenza genome from Switzerland allows deeper insights into host adaptation during the 1918 flu pandemic in Europe.BMC biology · 2025Article
- DUOX2 regulates secreted factors in virus-infected respiratory epithelial cells that contribute to neutrophil attraction and activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- ZBP1/DAI-Dependent Cell Death Pathways in Influenza A Virus Immunity and Pathogenesis.Current topics in microbiology and immunology · 2023Article
- Archival influenza virus genomes from Europe reveal genomic variability during the 1918 pandemic.Nature communications · 2022Article
- Understanding the Variability of Certain Biological Properties of H1N1pdm09 Influenza Viruses.Vaccines · 2022Article
- Amino Acid Mutations in Hemagglutinin-Neuraminidase Enhance the Virulence and Pathogenicity of the Genotype III Newcastle Disease Vaccine Strain After Intravenous Inoculation.Frontiers in veterinary science · 2022Article
- Innate immune responses at the asymptomatic stage of influenza A viral infections of Streptococcus pneumoniae colonized and non-colonized mice.Scientific reports · 2021Article
- Diversity in heat shock protein families: functional implications in virus infection with a comprehensive insight of their role in the HIV-1 life cycle.Cell stress & chaperones · 2021Review
- Human Properdin Released By Infiltrating Neutrophils Can Modulate Influenza A Virus Infection.Frontiers in immunology · 2021Article
- Effect of ORF7 of SARS-CoV-2 on the Chemotaxis of Monocytes and Neutrophils In Vitro.Disease markers · 2021Article
- Peripheral blood T cells response in human parainfluenza virus-associated lower respiratory tract infection in children.Saudi journal of biological sciences · 2020Article
- Article
- Hemagglutinin Cleavability, Acid Stability, and Temperature Dependence Optimize Influenza B Virus for Replication in Human Airways.Journal of virology · 2019Article
- NP and NS1 proteins of H5N1 virus significantly upregulated IFITM1, IFITM2, and IFITM3 in A549 cells.African health sciences · 2019Article
- A Role for Neutrophils in Viral Respiratory Disease.Frontiers in immunology · 2017Review
- Amino Acid Substitution K470R in the Nucleoprotein Increases the Virulence of H5N1 Influenza A Virus in Mammals.Frontiers in microbiology · 2017Article
- Respiratory viral infections and host responses; insights from genomics.Respiratory research · 2016Review
- The 1918 Influenza Virus PB2 Protein Enhances Virulence through the Disruption of Inflammatory and Wnt-Mediated Signaling in Mice.Journal of virology · 2015Article
- Lower Respiratory Tract Infection of the Ferret by 2009 H1N1 Pandemic Influenza A Virus Triggers Biphasic, Systemic, and Local Recruitment of Neutrophils.Journal of virology · 2015Article
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
The 1918 pandemic influenza virus was the most devastating infectious agent in human history, causing fatal pneumonia and an estimated 20 to 50 million deaths worldwide. Previous studies indicated a prominent role of the hemagglutinin (HA) gene in efficient replication and high virulence of the 1918 virus in mice. It is, however, still unclear whether the high replication ability or the 1918 influenza virus HA gene is required for 1918 virus to exhibit high virulence in mice. Here, we examined the biological properties of reassortant viruses between the 1918 virus and a contemporary human H1N1 virus (A/Kawasaki/173/2001 [K173]) in a mouse model. In addition to the 1918 influenza virus HA, we demonstrated the role of the viral RNA replication complex in efficient replication of viruses in mouse lungs, whereas only the HA gene is responsible for lethality in mice. Global gene expression profiling of infected mouse lungs revealed that the 1918 influenza virus HA was sufficient to induce transcriptional changes similar to those induced by the 1918 virus, despite difference in lymphocyte gene expression. Increased expression of genes associated with the acute-phase response and the protein ubiquitination pathway were enriched during infections with the 1918 and 1918HA/K173 viruses, whereas reassortant viruses bearing the 1918 viral RNA polymerase complex induced transcriptional changes similar to those seen with the K173 virus. Taken together, these data suggest that HA and the viral RNA polymerase complex are critical determinants of Spanish influenza pathogenesis, but only HA, and not the viral RNA polymerase complex and NP, is responsible for extreme host responses observed in mice infected with the 1918 influenza virus.
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