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

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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.

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In late March 2009, an outbreak of a respiratory illness later proved to be caused by novel swine-origin influenza A (H1N1) virus (S-OIV) was identified in Mexico. We describe the clinical and epidemiologic characteristics of persons hospitalized for pneumonia at the national tertiary hospital for respiratory illnesses in Mexico City who had laboratory-confirmed S-OIV infection, also known as swine flu. We used retrospective medical chart reviews to collect data on the hospitalized patients. S-OIV infection was confirmed in specimens with the use of a real-time reverse-transcriptase-polymerase-chain-reaction assay. From March 24 through April 24, 2009, a total of 18 cases of pneumonia and confirmed S-OIV infection were identified among 98 patients hospitalized for acute respiratory illness at the National Institute of Respiratory Diseases in Mexico City. More than half of the 18 case patients were between 13 and 47 years of age, and only 8 had preexisting medical conditions. For 16 of the 18 patients, this was the first hospitalization for their illness; the other 2 patients were referred from other hospitals. All patients had fever, cough, dyspnea or respiratory distress, increased serum lactate dehydrogenase levels, and bilateral patchy pneumonia. Other common findings were an increased creatine kinase level (in 62% of patients) and lymphopenia (in 61%). Twelve patients required mechanical ventilation, and seven died. Within 7 days after contact with the initial case patients, a mild or moderate influenza-like illness developed in 22 health care workers; they were treated with oseltamivir, and none were hospitalized. S-OIV infection can cause severe illness, the acute respiratory distress syndrome, and death in previously healthy persons who are young to middle-aged. None of the secondary infections among health care workers were severe. 2009 Massachusetts Medical Society

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Author and article information

Contributors

Eric O. Freed: Role: Academic Editor

Journal

Journal ID (nlm-ta): Viruses

Journal ID (iso-abbrev): Viruses

Journal ID (publisher-id): viruses

Title: Viruses

Publisher: MDPI

ISSN (Electronic): 1999-4915

Publication date (Electronic): 02 February 2016

Publication date Collection: February 2016

Volume: 8

Issue: 2

Electronic Location Identifier: 33

Affiliations

[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; tangjy@ 123456lzu.edu.cn (J.T.); Santanu.biswas@ 123456fda.hhs.gov (S.B); Jiangqin.zhao@ 123456fda.hhs.gov (J.Z.); Krishnakumar.devada@ 123456fda.hhs.gov (K.D.)

[2 ]Division of Viral Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD 20993, USA; zhiping.ye@ 123456fda.hhs.gov

Author notes

[* ]Correspondence: xue.wang@ 123456fda.hhs.gov (X.W.); indira.hewlett@ 123456fda.hhs.gov (I.H.); Tel: +1-240-402-8237 (X.W.); Fax: +1-301-595-1233 (X.W.)

[†]

These authors contributed equally to this work.

[‡]

Current address: Department of Immunology, School of Basic Medical Science, Lanzhou University, Lanzhou, Gansu 730000, China.

Article

Publisher ID: viruses-08-00033

DOI: 10.3390/v8020033

PMC ID: 4776188

PubMed ID: 26848681

SO-VID: 8e5e25b3-9455-40cd-a9c3-016361f6f9fe

License:

This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

History

Date received : 18 September 2015

Date accepted : 15 January 2016

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