Abstract
Coinfection with hepatitis C virus (HCV) influences HIV reservoir size. However, it is unknown whether this coinfection also induces a higher provirus transcription. Viral transcription is promoted by synergy between cellular factors such as NF-κB and the viral regulator Tat. The impact of HCV coinfection on HIV provirus transcription was analyzed in resting (r)CD4 T+ cells (CD3+CD4+CD25-CD69-HLADR-) and rCD4 T cells-depleted PBMCs (rCD4 T- PBMCs) from a multicenter cross-sectional study of 115 cART-treated HIV patients: 42 HIV+/HCV+ coinfected individuals (HIV+/HCV+), 34 HIV+ patients with HCV spontaneous clearance (HIV+/HCV−) and 39 HIV patients (HIV+). Viral transcription was assessed in total RNA through the quantification of unspliced, single spliced, and multiple spliced viral mRNAs by qPCR. Linear correlations between viral reservoir size and viral splicing were determined. A 3-fold increase of multiple spliced transcripts in rCD4 T+ cells of HIV+/HCV+ patients was found compared to HIV+ individuals (p < 0.05). As Tat is synthesized by multiple splicing, the levels of Tat were also quantified in these patients. Significant differences in single and multiple spliced transcripts were also observed in rCD4 T- PBMCs. Levels of multiple spliced mRNAs were increased in rCD4 T+ cells isolated from HIV+/HCV+ subjects, which could indicate a higher Tat activity in these cells despite their resting state.
Highlights
According to the United Nation’s HIV/AIDS program UNAIDS, the human immunodeficiency virus type 1 (HIV) affects 37.9 million people in 2018 and is one of the most prevalent and deadly infections worldwide [1]
Our group recently determined that HIV/Hepatitis C virus (HCV) coinfection enhances the size of HIV proviral DNA in patients exposed to HCV contrasting to HIV monoinfected subjects, in both HCV spontaneous viral clarifiers (HIV+/HCV−) and HCV chronically infected individuals (HIV+/HCV+) [9]
Patients were categorized into 3 groups according to their HCV status: (1) HIV+ monoinfected group, formed by patients not exposed to HCV; (2) HIV+/HCV− group, whose patients were HIV+ and had been exposed to HCV but experienced HCV spontaneous viral clearance during the first 6 months after HCV infection; and (3) HIV+/HCV+ group, constituted by patients infected with HIV on cART and active HCV−chronic infection naïve to any HCV treatment
Summary
According to the United Nation’s HIV/AIDS program UNAIDS, the human immunodeficiency virus type 1 (HIV) affects 37.9 million people in 2018 and is one of the most prevalent and deadly infections worldwide [1]. Hepatitis C virus (HCV) infection remains a major health problem with 71 million chronically infected individuals [4]. Our group recently determined that HIV/HCV coinfection enhances the size of HIV proviral DNA in patients exposed to HCV contrasting to HIV monoinfected subjects, in both HCV spontaneous viral clarifiers (HIV+/HCV−) and HCV chronically infected individuals (HIV+/HCV+) [9]. It is unknown whether coinfection affects proviral transcription and if this could significantly affect the strategies for the elimination of HIV-1 reservoir in these subjects
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