ArticleScientific reports2015
Early apoptosis of porcine alveolar macrophages limits avian influenza virus replication and pro-inflammatory dysregulation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Gasdermin E is dispensable for H1N1 influenza virus pathogenesis in mice.Microbiology spectrum · 2026Article
- Alveolar Macrophages in Viral Respiratory Infections: Sentinels and Saboteurs of Lung Defense.International journal of molecular sciences · 2025Review
- Sialic Acid Receptor Specificity in Mammary Gland of Dairy Cattle Infected with Highly Pathogenic Avian Influenza A(H5N1) Virus.Emerging infectious diseases · 2024Article
- Amino acid 138 in the HA of a H3N2 subtype influenza A virus increases affinity for the lower respiratory tract and alveolar macrophages in pigs.PLoS pathogens · 2024Article
- The role of PB1-F2 in adaptation of high pathogenicity avian influenza virus H7N7 in chickens.Veterinary research · 2024Article
- Impact of swine influenza A virus on porcine reproductive and respiratory syndrome virus infection in alveolar macrophages.Frontiers in veterinary science · 2024Article
- Porcine γδ T cells express cytotoxic cell-associated markers and display killing activity but are not selectively cytotoxic against PRRSV- or swIAV-infected macrophages.Frontiers in immunology · 2024Article
- Influenza viral matrix 1 protein aggravates viral pathogenicity by inducing TLR4-mediated reactive oxygen species production and apoptotic cell death.Cell death & disease · 2023Article
- Alveolar Macrophages Participate in the Promotion of Influenza Virus Infection by Aflatoxin B1 at an Early Stage.Toxins · 2023Article
- Swine influenza virus triggers ferroptosis in A549 cells to enhance virus replication.Virology journal · 2022Article
- Comparative transcriptomics reveals small RNA composition and differential microRNA responses underlying interferon-mediated antiviral regulation in porcine alveolar macrophages.Frontiers in immunology · 2022Article
- Innate immune responses at the asymptomatic stage of influenza A viral infections of Streptococcus pneumoniae colonized and non-colonized mice.Scientific reports · 2021Article
- Assessment of replication of bovine herpesvirus type 4 in human glioblastoma and breast cancer cells as a potential oncolytic virus.Virus genes · 2021Article
- Swine MicroRNAsJournal of virology · 2020Article
- H7N9 influenza A virus activation of necroptosis in human monocytes links innate and adaptive immune responses.Cell death & disease · 2019Article
- The induction and consequences of Influenza A virus-induced cell death.Cell death & disease · 2018Review
- Evolution and Virulence of Influenza A Virus Protein PB1-F2.International journal of molecular sciences · 2017Review
- Selective replication of oncolytic virus M1 results in a bystander killing effect that is potentiated by Smac mimetics.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Influenza Virus Overcomes Cellular Blocks To Productively Replicate, Impacting Macrophage Function.Journal of virology · 2017Article
- Role of Autophagy and Apoptosis in the Postinfluenza Bacterial Pneumonia.BioMed research international · 2016Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Pigs are evidently more resistant to avian than swine influenza A viruses, mediated in part through frontline epithelial cells and alveolar macrophages (AM). Although porcine AM (PAM) are crucial in influenza virus control, their mode of control is unclear. To gain insight into the possible role of PAM in the mediation of avian influenza virus resistance, we compared the host effects and replication of two avian (H2N3 and H6N1) and three mammalian (swine H1N1, human H1N1 and pandemic H1N1) influenza viruses in PAM. We found that PAM were readily susceptible to initial infection with all five avian and mammalian influenza viruses but only avian viruses caused early and extensive apoptosis (by 6 h of infection) resulting in reduced virus progeny and moderated pro-inflammation. Full length viral PB1-F2 present only in avian influenza viruses is a virulence factor that targets AM for mitochondrial-associated apoptotic cell death. With the use of reverse genetics on an avian H5N1 virus, we found that full length PB1-F2 contributed to increased apoptosis and pro-inflammation but not to reduced virus replication. Taken together, we propose that early apoptosis of PAM limits the spread of avian influenza viruses and that PB1-F2 could play a contributory role in the process.
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