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Viruses 2016, 8(2), 33; doi:10.3390/v8020033

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

1
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
2
Division of Viral Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD 20993, USA
These authors contributed equally to this work.
Current address: Department of Immunology, School of Basic Medical Science, Lanzhou University, Lanzhou, Gansu 730000, China
*
Authors to whom correspondence should be addressed.
Academic Editor: Eric O. Freed
Received: 18 September 2015 / Revised: 12 January 2016 / Accepted: 15 January 2016 / Published: 2 February 2016
View Full-Text   |   Download PDF [631 KB, uploaded 2 February 2016]   |  

Abstract

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. View Full-Text
Keywords: HIV-1; pandemic influenza A (H1N1) virus; apoptosis; CD4; replication HIV-1; pandemic influenza A (H1N1) virus; apoptosis; CD4; replication
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Wang, X.; Tan, J.; Biswas, S.; Zhao, J.; Devadas, K.; Ye, Z.; Hewlett, I. Pandemic Influenza A (H1N1) Virus Infection Increases Apoptosis and HIV-1 Replication in HIV-1 Infected Jurkat Cells. Viruses 2016, 8, 33.

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