Assessment of Key Elements in the Innate Immunity System Among Patients with HIV, HCV, and Coinfections of HIV/HCV

Curr HIV Res. 2020;18(3):194-200. doi: 10.2174/1570162X18999200325162533.

Abstract

Background: Coinfection of Hepatitis C virus (HCV) with human immunodeficiency virus (HIV) has a higher risk of mortality than HCV or HIV monoinfection. HCV and HIV infections are specified by systemic inflammation, but the inflammation process in HCV/HIV coinfection is much complicated and is not well characterized.

Objective: The aim of this study was to analyze the expression of TLR-3, TLR-7, IL-10, IFN-1 (IFN-α, IFN-β), and TNF-α in HIV, HCV and HIV/HCV co-infected patients.

Methods: Forty-five patients including HIV group (n=15), HCV group (n=15), HIV/HCV coinfection group (n=15) and healthy control group (n=15) participated. Peripheral blood mononuclear cells (PBMCs) were obtained. PBMC-RNA, HCV and HIV RNA were extracted from all subjects and cDNA was synthesized. The viral load analyzed by reverse transcription-quantitative PCR (RT-qPCR), and the expression levels of IFN-α, IFN-β, TLR-3, TLR-7, TNF, and IL-10 mRNA were quantified in PBMCs.

Results: The levels of IFN-I, IL-10, and TNF-α were overexpressed in all patients' groups (p<0.05), TLR-7 was upregulated in all groups, but this upregulation was not statistically significant (p>0.05). TLR-3 showed a decrease in all patient groups (p<0.05). The statistical analysis demonstrated that TLR-3 has a negative correlation with HIV load, whereas other genes positively correlated with HIV load. In addition, TLR-3, TNF-α, and IFN-I were negatively correlated with HCV load, whereas TLR-7 and IL-10 s were positively correlated with HCV load.

Conclusion: Our results showed a significant relationship between the expression level of innate immunity genes and inflammation in HCV, HIV, and HIV/HCV coinfected patients.

Keywords: Coinfection; HCV; HIV; IFN-I; IL-10; TLR-3; TLR-7; TNF-α..

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Case-Control Studies
  • Coinfection
  • Female
  • Gene Expression Regulation
  • HIV / genetics
  • HIV / immunology*
  • HIV Infections / genetics
  • HIV Infections / immunology*
  • HIV Infections / pathology
  • HIV Infections / virology
  • Hepacivirus / genetics
  • Hepacivirus / immunology*
  • Hepatitis C, Chronic / genetics
  • Hepatitis C, Chronic / immunology*
  • Hepatitis C, Chronic / pathology
  • Hepatitis C, Chronic / virology
  • Host-Pathogen Interactions / genetics
  • Host-Pathogen Interactions / immunology
  • Humans
  • Immunity, Innate*
  • Inflammation
  • Interferon-alpha / genetics
  • Interferon-alpha / immunology
  • Interferon-beta / genetics
  • Interferon-beta / immunology
  • Interleukin-10 / genetics
  • Interleukin-10 / immunology
  • Male
  • Middle Aged
  • RNA, Viral / genetics
  • RNA, Viral / immunology*
  • Toll-Like Receptor 3 / genetics
  • Toll-Like Receptor 3 / immunology
  • Toll-Like Receptor 7 / genetics
  • Toll-Like Receptor 7 / immunology
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology
  • Viral Load / genetics
  • Viral Load / immunology

Substances

  • IL10 protein, human
  • Interferon-alpha
  • RNA, Viral
  • TLR3 protein, human
  • TLR7 protein, human
  • Toll-Like Receptor 3
  • Toll-Like Receptor 7
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Interferon-beta