ArticleBioMed research international2013
Dose- and time-dependent apoptosis induced by avian H9N2 influenza virus in human cells.
Article in BioMed research international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- The applications of live attenuated influenza a virus with modified NS1 gene.Molecular therapy. Nucleic acids · 2025Review
- RETRACTION: Dose- and Time-Dependent Apoptosis Induced by Avian H9N2 Influenza Virus in Human Cells.BioMed research international · 2025Article
- Erythromycin, retapamulin, pyridoxine, folic acid, and ivermectin inhibit cytopathic effect, papain-like protease, and MFrontiers in cellular and infection microbiology · 2023Article
- Apoptosis in field and experimental cases of avian influenza HVeterinary research forum : an international quarterly journal · 2022Article
- Schmallenberg virus induces apoptosis in Vero cell line via extrinsic and intrinsic pathways in a time and dose dependent manner.The Journal of veterinary medical science · 2019Article
- A brief summary of the epidemiology and genetic relatedness of avian influenza H9N2 virus in birds and mammals in the Middle East and North Africa.Epidemiology and infection · 2017Review
- Interfering With Lipid Raft Association: A Mechanism to Control Influenza Virus Infection ByIranian journal of pharmaceutical research : IJPR · 2017Article
- Proteomic Analysis of Differential Expression of Cellular Proteins in Response to Avian H9N2 Virus Infection of A549 Cells.Frontiers in microbiology · 2016Article
- Influenza A Virus and Influenza B Virus Can Induce Apoptosis via Intrinsic or Extrinsic Pathways and Also via NF-κB in a Time and Dose Dependent Manner.Biochemistry research international · 2016Article
- Inactivated Sendai virus strain Tianjin induces apoptosis in breast cancer MCF-7 cells by promoting caspase activation and Fas/FasL expression.Cancer biotherapy & radiopharmaceuticals · 2015Article
- Expression of Factor X in BHK-21 Cells Promotes Low Pathogenic Influenza Viruses Replication.Advances in virology · 2015Article
- Necrotic Response to Low Pathogenic H9N2 Influenza Virus in Chicken Hepatoma Cells.Jundishapur journal of microbiology · 2015Article
Corrections and comments
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To understand human response to avian H9N2 influenza, we investigated the effects of the viral infection on A549, HepG2, and HeLa cells at low and high MOIs. To identify virus-host interplay, expression of Mx and NP genes was measured in the cells supernatants. Cell viability and apoptosis were evaluated by MTT assay, DNA fragmentation, and florescent staining. The virus titration and NP gene transcript levels indicate lower susceptibility of HeLa cell to H9N2 replication than other cells. Although H9N2 did produce a faster CPE in HepG2, high dose of the virus induced apoptosis within early stage of A549 infection. The DNA laddering was enhanced in the cell correlated with increase in virus transcripts. The undetectable to different regulation levels of Mx gene were observed in response to H9N2 infection suggesting that an insufficient antiviral defense in the noncompetent-IFN HepG2 cell promotes efficient viral replication. These results showed that the permissivity of HepG2 for H9N2 is comparable with A549; however, liver cells are not target tissue respond to the infection. These data revealed that the H9N2 virus induced apoptosis signaling via mitochondrial pathway in human alveolar epithelial cells, indicating that the induction may be associated with a dose-dependent manner.
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Registered trials
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.