Khurana Sandhya, Krementsov Dimitry N, de Parseval Aymeric, Elder John H, Foti Michelangelo, Thali Markus
Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, VT 05405, USA.
J Virol. 2007 Nov;81(22):12630-40. doi: 10.1128/JVI.01255-07. Epub 2007 Sep 12.
Directed release of human immunodeficiency virus type 1 (HIV-1) into the cleft of the virological synapse that can form between infected and uninfected T cells, for example, in lymph nodes, is thought to contribute to the systemic spread of this virus. In contrast, influenza virus, which causes local infections, is shed into the airways of the respiratory tract from free surfaces of epithelial cells. We now demonstrate that such differential release of HIV-1 and influenza virus is paralleled, at the subcellular level, by viral assembly at different microsegments of the plasma membrane of HeLa cells. HIV-1, but not influenza virus, buds through microdomains containing the tetraspanins CD9 and CD63. Consequently, the anti-CD9 antibody K41, which redistributes its antigen and also other tetraspanins to cell-cell adhesion sites, interferes with HIV-1 but not with influenza virus release. Altogether, these data strongly suggest that the bimodal egress of these two pathogenic viruses, like their entry into target cells, is guided by specific sets of host cell proteins.
例如，在淋巴结中，人类免疫缺陷病毒1型（HIV-1）定向释放到受感染和未受感染的T细胞之间可形成的病毒学突触裂隙中，被认为有助于该病毒的全身传播。相比之下，引起局部感染的流感病毒则从上皮细胞的自由表面释放到呼吸道的气道中。我们现在证明，在亚细胞水平上，HIV-1和流感病毒的这种差异释放与它们在HeLa细胞质膜的不同微区进行病毒组装是平行的。HIV-1而非流感病毒通过含有四跨膜蛋白CD9和CD63的微区出芽。因此，抗CD9抗体K41可将其抗原以及其他四跨膜蛋白重新分布到细胞间粘附位点，从而干扰HIV-1的释放，但不干扰流感病毒的释放。总之，这些数据有力地表明，这两种致病病毒的双峰释放，就像它们进入靶细胞一样，是由特定的宿主细胞蛋白组所引导的。
