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Gene expression profiling of CD4+ T cells in treatment-naive HIV, HCV mono- or co-infected Chinese

Lina Yi13, Jin Zhao12, Jing Lu3, Ying Chen1, Lin Chen2, Jinquan Cheng2, Yan Sun4, Zhi Li4, Ruotin Men5, Li Yang5, Hsiangfu Kung1, Zhengrong Yang2* and Ming-liang He16*

Author Affiliations

1 Stanley Ho Center for Emerging Infectious Diseases, and Li Ka Shing Institute of Health Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China

2 Shenzhen Center for Disease Control and Prevention, Shenzhen, China

3 Guangdong Provincial Institution of Public Health, Guangdong Provincial Center for Diseases Control and Prevention, Guangzhou, China

4 College of Life Science, Shanxi Normal University, Xi’an, China

5 Department of Gastroenterology, Huaxi Medical College, Sichuan University, Sichuan, China

6 Prince Wales Hospital, Faculty of Medicine, The Chinese University of Hong Kong, Li Ka Shing Medical Science Bldg, Hong Kong, China

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Virology Journal 2014, 11:27  doi:10.1186/1743-422X-11-27

Published: 13 February 2014



Because of the shared transmission routes, co-infection with human immunodeficiency virus (HIV) and hepatitis C virus (HIV) is very common. Accumulated clinical evidence showed that one could alter the infectious course of the other virus in HIV and HCV co-infected individuals. However, little is known on the molecular basis of HIV/HCV interactions and their modulations on hosts.


In this study, treatment-naive HIV, HCV mono-/co-infected individuals with CD4+ T cell counts >300/μl were recruited and their gene expression profiles were investigated by microarray assays. The differentially expressed genes were identified and validated by quantitative real-time PCR (qRT-PCR). To further understand the biological meanings of the gene expression profiles in these three groups, GSEA analysis (version 2.0, Broad Institute webcite) was performed.


By gene set enrichment analysis, we revealed that gene sets of cell cycle progression, innate immune response and some transcription factors in CD4+ T cells were mainly affected by HIV; while genes associated with GPCR signaling were the major targets of HCV. Metabolic pathways were modulated by both HCV and HIV viruses.


This study for the first time offers gene profiling basis for HCV/HIV mono-/co- infections in human beings. HIV infection displayed the great impact on transcription profile of CD4+ T cells in HIV/HCV co-infected individuals. Genes related to cell cycle arrest were significantly mediated by HIV which may lead to dysfunction of CD4+ T cells and acceleration of HCV-related disease progression in the co-infections.

HIV; HCV; Co-infection; Microarray; CD4+ T cells