Pandemic Influenza A (H1N1) Virus Infection Increases Apoptosis and HIV-1 Replication in HIV-1 Infected Jurkat Cells

Viruses

Zhiping Ye¹  Jiying Tan²  Jiangqin Zhao²  Santanu Biswas²  Indira Hewlett²  Krishnakumar Devadas²  Xue Wang² 

[1] Division of Viral Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD 20993, USA;Lab of Molecular Virology, Division of Emerging and Transfusion Transmitted Diseases, CBER/FDA, Building 72, Rm 4322, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA;

关键词: HIV-1;    pandemic influenza A (H1N1) virus;    apoptosis;    CD4;    replication;   

DOI  :  10.3390/v8020033

来源: DOAJ

【 摘 要 】

Influenza virus infection has a significant impact on public health, since it is a major cause of morbidity and mortality. It is not well-known whether influenza virus infection affects cell death and human immunodeficiency virus (HIV)-1 replication in HIV-1-infected patients. Using a lymphoma cell line, Jurkat, we examined the in vitro effects of pandemic influenza A (H1N1) virus (pH1N1) infection on cell death and HIV-1 RNA production in infected cells. We found that pH1N1 infection increased apoptotic cell death through Fas and Bax-mediated pathways in HIV-1-infected Jurkat cells. Infection with pH1N1 virus could promote HIV-1 RNA production by activating host transcription factors including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-ĸB), nuclear factor of activated T-cells (NFAT) and activator protein 1 (AP-1) through mitogen-activated protein kinases (MAPK) pathways and T-cell antigen receptor (TCR)-related pathways. The replication of HIV-1 latent infection could be reactivated by pH1N1 infection through TCR and apoptotic pathways. These data indicate that HIV-1 replication can be activated by pH1N1 virus in HIV-1-infected cells resulting in induction of cell death through apoptotic pathways.

【 授权许可】

Unknown