HIV-1 Transcription but Not Intact Provirus Levels are Associated With Systemic Inflammation. (19th October 2020)

• Record Type: Journal Article
• Authors: Olson, Alex; Coote, Carolyn; Snyder-Cappione, Jennifer E; Lin, Nina; Sagar, Manish
• Is Part Of: Journal of infectious diseases. Volume 223:Number 11(2021)
• Page Start: 1934
• Page End: 1942
• Publication Date: 2020-10-19
• Subjects: HIV-1 latency -- accelerated aging -- cell-associated HIV -- inflammation -- viral transcription; Communicable diseases -- Periodicals; Diseases -- Causes and theories of causation -- Periodicals; Medicine -- Periodicals; Communicable Diseases -- Periodicals; Electronic journals; 616.9
• DOI: 10.1093/infdis/jiaa657
• Languages: English
• ISSNs: 0022-1899

Abstract

Abstract: Individuals infected with human immunodeficiency virus (HIV) 1 have increased inflammation, which has been associated with age-associated diseases. Plasma markers, cell-associated virus levels, and ability to stimulate RNA transcription in latently infected cell lines was examined in younger and older HIV-1–infected individuals with suppressed virus. Cell-associated RNA, but not intact provirus level, had positive correlation with plasma D-dimer levels. Compared with the younger group, the older group had higher D-dimer levels and a trend toward more cell-associated RNA but similar levels of intact proviruses. Even though all measured inflammatory markers were relatively higher in the older group, this greater inflammation did not induce more HIV-1 transcription in latently infected cell lines. Inflammation and HIV-1 RNA expression increase with age despite similar levels of intact infectious HIV DNA. While plasma inflammation is correlated with HIV-1 RNA expression in peripheral blood mononuclear cells, it does not induce HIV-1 transcription in latently infected cell lines. Abstract : Plasma inflammation increases with aging in treated people with human immunodeficiency virus (HIV), is associated with intracellular HIV-1 RNA levels but not with the number of intact infectious proviruses, and does not stimulate greater HIV-1 RNA transcription in cell lines.