Simian-Human immunodeficiency viruses expressing chimeric subtype B/C Vpu proteins demonstrate the importance of the amino terminal and transmembrane domains in the rate of CD4+ T cell loss in macaques

被引:3
作者
Ruiz, Autumn [1 ]
Schmitt, Kimberly [1 ]
Culley, Nathan [2 ]
Stephens, Edward B. [1 ]
机构
[1] Univ Kansas, Med Ctr, Dept Microbiol Mol Genet & Immunol, Kansas City, KS 66160 USA
[2] Univ Kansas, Med Ctr, Lab Anim Resources, Kansas City, KS 66160 USA
关键词
Vpu; Simian-human immunodeficiency virus; SHIV; Pathogenesis; Transmembrane domain; CD4+T cell loss; Subtype C HIV-1; Chimeric Vpu protein; HIV-1; GROUP-O; DOWN-REGULATION; HUMAN TETHERIN; TYPE-1; B VPU; BST-2; RELEASE; DEGRADATION; ENV; IDENTIFICATION;
D O I
10.1016/j.virol.2012.10.030
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Previously, we reported that simian-human immunodeficiency viruses expressing either the lab adapted subtype B (SHIVKU-1bMC33) or subtype C (SHIVSCVpu) Vpu proteins of human immunodeficiency virus type 1 (HIV-1) had different rates of CD4(+) T cell loss following inoculation into macaques. In this study, we have generated SHIVs that express either the subtype B or subtype C N-terminal (NTD) and transmembrane (TMD) domains and the opposing cytoplasmic domain (SHIVVpuBc, SHIVVpuCB). In culture systems, SHIVVpuBc replicated faster than SHIVVpuCB while both proteins exhibited similar ability to down-modulate CD4 surface expression. Following inoculation into macaques, SHIVVpuBC resulted in rapid CD4(+) T cell loss similar to the parental SHIVKU-1bMC33, while the rate of CD4(+) T cell loss in those inoculated with SHIVVpuCB 03 was intermediate of SHIVSCVpu. and SHIVKU-1bMC33. These results emphasize the importance of the Vpu NTD/TMD region in the rate of CD4(+) T cell loss in the pathogenic X4 SHIV/macaque model. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:395 / 405
页数:11
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