Underlying Pathophysiology of HCV Infection in HIV-Positive Drug Users

Balasubramanian, Anuradha; Groopman, Jerome E.; Ganju, Ramesh K.

doi:10.1300/j069v27n02_09

Cited by 7 publications

(5 citation statements)

References 80 publications

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“…Analysis of gene expression profiles in the HCV/HIV mono-infected or co-infected patients would provide a unique opportunity to understand the mechanisms. It is reported that factors, such as direct viral effects, the immunologic alterations especially the specific T-cell response, have played important roles in the disease progression [ 11 - 13 ]. CD4 + T cells, the major HIV target cells, also play an essential role in HCV clearance [ 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

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

Liu

Zhao

Lü

et al. 2014

Virol J

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BackgroundBecause 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.MethodsIn 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 http://www.broad.mit.edu/gsea) was performed.ResultsBy 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.ConclusionsThis 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.

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Section: Introductionmentioning

confidence: 99%

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

Liu

Zhao

Lü

et al. 2014

Virol J

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“…Earlier studies showed HCV infection stimulates cytokine production. [91] However, with HCV infection and alcohol intake, T h 1 and not T h 2 cytokines were elevated. [297] Up-regulation of intrahepatic T h 1 cytokines, IL-2 and IFNg, and downregulation of T h 2 and in serum, IL-10 increase was detected in prior studies.…”

Section: Drug Abuse and Immunementioning

confidence: 96%

Molecular and Contextual Markers of Hepatitis C Virus and Drug Abuse

et al. 2009

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The spread of hepatitis C virus (HCV) infection involves a complex interplay of social risks, and molecular factors of both virus and host. Injection drug abuse is the most powerful risk factor for HCV infection, followed by sexual transmission and additional non-injection drug abuse factors such as co-infection with other viruses and barriers to treatment. It is clearly important to understand the wider context in which the factors related to HCV infection occur. This understanding is required for a comprehensive approach leading to the successful prevention, diagnosis, and treatment of HCV. An additional consideration is that current treatments and advanced molecular methods are generally unavailable to socially disadvantaged patients. Thus, the recognition of behavioral/social, viral, and host factors as components of an integrated approach to HCV is important to help this vulnerable group. Equally important, this approach is key to the development of personalized patient treatment – a significant goal in global healthcare. In this review, we discuss recent findings concerning the impact of drug abuse, epidemiology, social behavior, virology, immunopathology, and genetics on HCV infection and the course of disease.

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“…Mechanisms of accelerated disease progression in HIV/HCV-coinfection have not been fully determined. However, disturbances in virus-specific T cell responses via altered activity of regulatory T cells (T reg ) are thought to play an important role [6][7][8] in infections caused by HIV, HCV, and herpes virus [9][10][11][12]. Prior work has shown T reg expansion in the course of HIV and/or HCV infection [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Effects of Pegylated Interferon Alpha and Ribavirin (pegIFN-α/RBV) Therapeutic Approach on Regulatory T Cells in HCV-Monoinfected and HCV/HIV-Coinfected Patients

Grubczak

Grzeszczuk

Groth

et al. 2021

Viruses

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Approximately 25% of HIV-infected patients are co-infected with HCV. Notably, the burden of HCV infection (e.g., viral persistence, viral load, or HCV-related liver symptoms) is more pronounced in the presence of HIV co-infection. However, to date, the underlying immune mechanisms accounting for accelerated disease progression in HIV/HCV-coinfected individuals have not been described in sufficient detail. We hypothesized that regulatory T cells (Treg) bearing potent immunosuppressive capacities could not only play a substantial role in the pathogenesis of HCV/HIV coinfection but also modulate the response to the standard anti-viral therapy. Materials and Methods: To this end, we studied alterations in frequencies of Treg cells in correlation with other Treg-related and virus-related parameters in both HCV and HCV/HIV-infected patients subjected to standard pegIFN-α/RBV therapy. Results: Notably, we found that pegIFN-α/RBV therapy significantly increased levels of Treg cells in HCV-infected but not in HIV/HCV-coinfected individuals. Furthermore, HIV/HCV-coinfection was demonstrated to inhibit expansion of regulatory T cells during anti-viral treatment; thus, it might probably be responsible for viral persistence and HCV-related liver damage. Conclusions: Therapy with pegIFN-α/RBV demonstrated a significant effect on regulatory T cells in the course of HIV and/or HCV infection indicating a crucial role in the anti-viral immune response.

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Underlying Pathophysiology of HCV Infection in HIV-Positive Drug Users

Cited by 7 publications

References 80 publications

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

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

Molecular and Contextual Markers of Hepatitis C Virus and Drug Abuse

Effects of Pegylated Interferon Alpha and Ribavirin (pegIFN-α/RBV) Therapeutic Approach on Regulatory T Cells in HCV-Monoinfected and HCV/HIV-Coinfected Patients

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