Department of Molecular Virology, National AIDS Research Institute, G-73 MIDC, Bhosari, Pune, India.
Virus Res. 2012 Dec;170(1-2):154-8. doi: 10.1016/j.virusres.2012.08.020. Epub 2012 Sep 4.
Natural loss of L35Y36 residues in ALIX binding site of HIV-1 subtype C was found to prevent the p6 gag-ALIX interaction. Over expression of ALIX 364-716 (V-domain) unlike pNL4.3 (subtype B), also did not inhibit the release of chimeric pNL4.3 expressing subtype C p6 late domain. Loss of V domain binding consequently affected the ALIX mediated particle release in the absence of PTAP/TSG101 pathway. Our data indicated absence of LYPXnL/ALIX pathway in HIV-1 subtype C.
在 HIV-1 亚型 C 中发现，ALIX 结合位点中 L35Y36 残基的自然缺失可阻止 p6 gag-ALIX 相互作用。与 pNL4.3（亚型 B）不同，过表达 ALIX 364-716（V 结构域）也不会抑制表达亚型 C p6 晚期结构域的嵌合 pNL4.3 的释放。因此，V 结构域结合的缺失会影响在没有 PTAP/TSG101 途径的情况下，ALIX 介导的颗粒释放。我们的数据表明 HIV-1 亚型 C 中不存在 LYPXnL/ALIX 途径。
