ArticleJundishapur journal of microbiology2015
Necrotic Response to Low Pathogenic H9N2 Influenza Virus in Chicken Hepatoma Cells.
Article in Jundishapur journal of microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- RETRACTION: Dose- and Time-Dependent Apoptosis Induced by Avian H9N2 Influenza Virus in Human Cells.BioMed research international · 2025Article
- Unveiling the intersection: ferroptosis in influenza virus infection.Virology journal · 2024Review
- Chloride Intracellular Channel Protein 1 (CLIC1) Is a Critical Host Cellular Factor for Influenza A Virus Replication.Viruses · 2024Article
- Ferroptosis in viral infection: a potential therapeutic target.Future microbiology · 2024Review
- Influenza viral matrix 1 protein aggravates viral pathogenicity by inducing TLR4-mediated reactive oxygen species production and apoptotic cell death.Cell death & disease · 2023Article
- Swine influenza virus triggers ferroptosis in A549 cells to enhance virus replication.Virology journal · 2022Article
- Innate immune sensing of influenza A viral RNA through IFI16 promotes pyroptotic cell death.iScience · 2022Article
- Abdominal and Pelvic Organ Failure Induced by Intraperitoneal Influenza A Virus Infection in Mice.Frontiers in microbiology · 2020Article
- The induction and consequences of Influenza A virus-induced cell death.Cell death & disease · 2018Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLimited knowledge about the molecular mechanism of avian influenza H9N2 virus pathogenicity in birds as well as human hosts has limited the development of effective control against the disease. To overcome this issue detailed understanding of the infectious characteristics of the virus in host cells should be obtained.
objectivesIn this study we examined the replication kinetics of H9N2 virus in a chicken hepatoma cell line to obtain insight into the pathogenesis of H9N2 viruses. MATERIALS AND
methodsThe kinetic replication of H9N2 influenza virus in chicken hepatoma and fibroblastic cells was studied in the presence and absence of supplemental trypsin. High viral titers observed in liver cells in a short time correlated with the degree of cytopathic effects. To determine whether the ultimate outcome of infection results in programmed cell death, the infected cells were observed by the cell viability assay, DNA fragmentation, caspase cascade activation, and quantified lactate dehydrogenase release.
resultsThe degree of viability was significantly reduced in infected hepatoma cells. Observations of caspase activation and cell DNA laddering in infected cells were not indicative of apoptosis. The infected hepatoma cells released lactate dehydrogenase, which is consistent with cell death by necrosis.
conclusionsTaken together, these data reveal that cellular protease of chicken liver cells allows the replication of high yields of H9N2 virus in the absence of trypsin and also cell death in the infected cells is due to necrosis.
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