Ulich C, Harrich D, Estes P, Gaynor R B
Division of Molecular Virology, Department of Medicine, University of Texas Southwestern Medical Center at Dallas, Texas 75235-8594, USA.
J Virol. 1996 Jul;70(7):4871-6. doi: 10.1128/JVI.70.7.4871-4876.1996.
Mutation of either of two critical human immunodeficiency virus type 1 (HIV-1) regulatory proteins, Tat and Rev, results in marked defects in viral replication. Thus, inhibition of the function of one or both of these proteins can significantly inhibit viral growth. In the present study, we constructed a novel transdominant Tat mutant protein and compared its efficiency in inhibiting HIV-1 replication with that of transdominant mutant Rev M10 when these proteins were stably expressed either alone or in combination in T-lymphocyte cell lines. The transdominant Tat mutant protein alone resulted in a modest inhibition of HIV replication, but it was able to enhance the ability of the M10 Rev mutant protein to inhibit HIV-1 replication. These results suggest a possible synergistic effect of these transdominant mutant proteins in inhibiting HIV-1 replication.
两种关键的1型人类免疫缺陷病毒(HIV-1)调节蛋白Tat和Rev中的任何一种发生突变,都会导致病毒复制出现明显缺陷。因此,抑制这两种蛋白中一种或两种的功能可显著抑制病毒生长。在本研究中,我们构建了一种新型的反式显性Tat突变蛋白,并将其在稳定表达于T淋巴细胞系时单独或联合抑制HIV-1复制的效率与反式显性突变Rev M10的效率进行了比较。单独的反式显性Tat突变蛋白对HIV复制有适度抑制作用,但它能够增强M10 Rev突变蛋白抑制HIV-1复制的能力。这些结果表明这些反式显性突变蛋白在抑制HIV-1复制中可能存在协同作用。