Comparison of miRNA Expression Profiles between HIV-1 and HIV-2 Infected Monocyte-Derived Macrophages (MDMs) and Peripheral Blood Mononuclear Cells (PBMCs)

Abstract

During the progression of HIV-1 infection, macrophage tropic HIV-1 that use the CCR5 co-receptor undergoes a change in co-receptor use to CXCR4 that is predominately T cell tropic. This change in co-receptor preference makes the virus able to infect T cells. HIV-2 is known to infect MDMs and T cells and is dual tropic. The aim of this study was to elucidate the differential expression profiles of host miRNAs and their role in cells infected with HIV-1/HIV-2. To achieve this goal, a comparative global miRNA expression profile was determined in human PBMCs and MDMs infected with HIV-1/HIV-2. Differentially expressed miRNAs were identified in HIV-1/HIV-2 infected PBMCs and MDMs using the next-generation sequencing (NGS) technique. A comparative global miRNA expression profile in infected MDMs and PBMCs with HIV-1 and HIV-2 identified differential expression of several host miRNAs. These differentially expressed miRNAs are likely to be involved in many signaling pathways, like the p53 signaling pathway, PI3K-Akt signaling pathways, MAPK signaling pathways, FoxO signaling pathway, and viral carcinogenesis. Thus, a comparative study of the differential expression of host miRNAs in MDMs and T cell in response to HIV-1 and HIV-2 infection will help us to identify unique biomarkers that can differentiate HIV-1 and HIV-2 infection.

Different HCV Exposure Drives Specific miRNA Profile in PBMCs of HIV Patients

“…Hypoxia directly influences viral proliferation, promoting or suppressing infectivity depending on the virus [ 57 ]. Similarly, Santanu et al 2020 also reported an alteration of the HIF-1 signaling pathway in the PBMCs of HIV-1 patients [ 28 ].…”

“…Among these putative miRNAs, we highlight the miR-126-5p, hsa-miR-34a-5p and hsa-miR-148b-3p, whose expression levels were significantly higher in HIV/HCV coinfected PBMCs compared to HC. The miR-126-5p hepatic expression has been associated with HCV viral load [ 26 ], the circulating hsa-miR-34a-5p promotes liver fibrosis in CHC [ 27 ], and the hsa-miR-148b-3p has been previously identified as dysregulated in PBMCs of HIV patients [ 28 ]. Although these miRNAs were also associated with the regulation of carcinogenesis and antitumor responses [ 29 , 30 ], we found them involved in the PI3K-Akt signaling pathway.…”

Oral Epithelial Cells Distinguish betweenCandidaSpecies with High or Low Pathogenic Potential through MicroRNA Regulation

“…Other than antifungal host responses, miR-4755 and miR-4677 deregulation was previously linked to bacterial stimuli ( 58 , 66 ), miR-1305, miR-627, miR-543, and miR-581 to viral challenge, and miR-12135 to parasitic infections ( 67 ). miR-1277 and miR-365 were associated with host responses upon both bacterial and viral infections ( 68 – 72 ). Thus, although fewer miRNA species could be coupled with C. parapsilosis infections than with C. albicans , the majority of these were confirmed regulators of antimicrobial responses.…”

Potential role of micro ribonucleic acids in screening for anal cancer in human papilloma virus and human immunodeficiency virus related malignancies

“…Few studies determined the expression of cellular miRNAs in HIV-infected cell lines (Table 2 ). Recently, Biswas et al [ 118 ] established a comparative global miRNA expression profile in human PBMC and MDMs infected with HIV-1/HIV-2. Differentially expressed miRNAs were identified in these cells.…”

“…Differentially expressed miRNAs were identified in these cells. Pathway analysis using Kyoto Encyclopedia of Genes and Genomes database showed that the deregulated miRNAs are likely to be involved in p53 signaling pathway, PI3K-Akt signaling pathways, Mitogen-activated protein kinase signaling pathways, FoxO signaling pathway, and NF-kappaB inhibitor signaling pathway, all of which play a role in carcinogenesis[ 118 , 119 ]. HIV Tat, Nef, and Vpr have been reported to alter the expression levels of many miRNAs and contribute to HIV pathogenesis (Table 3 ).…”