Assessment of key elements in the innate immunity system among patients with HIV, HCV, and coinfections of HIV/HCV

• Published in: Current HIV research
• Main Authors: Moradi, Maryam, Tabibzadeh, Alireza, Javanmard, Davod, Ghorbani, Saied, Bokharaei-Salim, Farah, Keivani, Hosein, Khazeni, Mohammad, Monavari, Seyed Hamid Reza
• Format: Journal Article
• Language: English
• Published: Netherlands 01.01.2020
• ISSN: 1873-4251
• DOI: 10.2174/1570162X18999200325162533

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 co-infection are much complicated and are not well characterized. 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. 1 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 were synthesis. The viral load analyzed by reverse transcription-quantitative PCR (RT-qPCR), as well, the expression levels of IFN-α, IFN-β, TLR-3, TLR-7, TNF, and IL-10 mRNA were quantified in PBMCs. The levels of IFN-I, IL-10, and TNF-α were overexpressed in all patients' groups (p<0.05), TLR-7 was up regulated in all groups, but this up regulation was not statistically significant (p>0.05). TLR-3 showed 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 IL10 s were positively correlated with HCV load. Our results showed a significant relationship between the expression level of innate immunity genes and inflammation in HCV, HIV, and HIV/HCV coinfected patients.