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.
Bacteremia in Malawian Children with Severe Malaria: Prevalence, Etiology, HIV Coinfection, and Outcome
