HIV-1 Tat implicated as a key factor in viral spread. (July 2008)

• Record Type: Journal Article
• Authors: Harrich, David; Apolloni, Ann; Warrilow, David
• Is Part Of: Future HIV therapy. Volume 2:Number 4(2008)
• Page Start: 323
• Page End: 326
• Publication Date: 2008-07
• Subjects: apoptosis -- HIV-1 -- oxygen -- pathogenesis -- Tat; HIV (Viruses) -- Treatment -- Periodicals; HIV (Viruses) -- Research -- Periodicals; 616.979206
• DOI: 10.2217/17469600.2.4.323
• Languages: English
• ISSNs: 1746-9600

Abstract

Evaluation of: Sahaf B, Atkuri K, Heydari K et al. : Culturing of human peripheral blood cells reveals unsuspected lymphocyte responses relevant to HIV disease. Proc. Natl Acad. Sci. USA 105, 5111––5116 (2008). Following HIV-1 infection, Tat is amongst the first of the viral proteins to be expressed. Tat is a potent transcription activator protein rocketing HIV-1 gene expression in the infected cells, thus ensuring that high levels of all viral proteins, including Tat, are made. HIV-1-infected cells secrete Tat into the periphery where it causes pathogenic effects, such as stimulation of Kaposi''s sarcoma, immune modulation and cytotoxicity. Previous studies have demonstrated that T lymphocytes can undergo apoptosis following exposure to exogenously added Tat. Here, Sahaf et al . caution that Tat had a dramatically different effect when it was added to cells cultured in incubators where the O2 tension was at physiological levels. Under these conditions, Tat actually stimulated T-lymphocyte proliferation and primed them for productive HIV-1 infection. Tat appears to have a new role during early HIV-1 disease by promoting viral spread. This curious and intriguing work has implications for our understanding of HIV-1 replication, and viral culture in general.