Rounseville M P, Lin H C, Agbottah E, Shukla R R, Rabson A B, Kumar A
Department of Biochemisty and Molecular Biology, George Washington University, Washington, DC 20037, USA.
Virology. 1996 Feb 15;216(2):411-7. doi: 10.1006/viro.1996.0077.
Human immunodeficiency virus type 1 (HIV-1) Tat-mediated trans-activation requires the structural integrity of TAR RNA and the cooperative interaction of human host cell proteins. The TAR domain, minimally required for tat response, includes the Tat binding pyrimidine bulge, the TAR RNA upper stem, and the loop sequences. However, little is known about the significance of the 5'-stem structure of TAR in the regulation of viral growth. We designed viral mutations, specifically in the TAR RNA lower stem structure, and studied their effects on the kinetics of viral growth in T-lymphocyte cell lines and in activated human peripheral blood mononuclear cells. Mutations that destabilized the lower TAR stem structure inhibited viral growth to various degrees in different CD4+ T-cells. These results suggest that the structural integrity of the lower stem structure of TAR plays an important role in viral growth, presumably by binding to specific host cell proteins that stabilize Tat-TAR interactions.
1型人类免疫缺陷病毒(HIV-1)的Tat介导的反式激活需要TAR RNA的结构完整性以及人类宿主细胞蛋白的协同相互作用。Tat反应所需的最小TAR结构域包括Tat结合嘧啶凸起、TAR RNA上茎和环序列。然而,关于TAR的5'茎结构在病毒生长调节中的意义知之甚少。我们设计了病毒突变,特别是在TAR RNA下茎结构中,并研究了它们对T淋巴细胞系和活化的人类外周血单核细胞中病毒生长动力学的影响。破坏TAR下茎结构稳定性的突变在不同的CD4+T细胞中不同程度地抑制了病毒生长。这些结果表明,TAR下茎结构的结构完整性在病毒生长中起重要作用,可能是通过与稳定Tat-TAR相互作用的特定宿主细胞蛋白结合来实现的。