Galectin-3 promotes HIV-1 budding via association with Alix and Gag p6

Sheng Fan Wang, Ching Han Tsao, Yu Ting Lin, Daniel K. Hsu, Meng Lin Chiang, Chia Hui Lo, Fan Ching Chien, Peilin Chen, Yi Ming Arthur Chen, Huan Yuan Chen, Fu Tong Liu

研究成果: 雜誌貢獻文章同行評審

36 引文 斯高帕斯(Scopus)

摘要

Galectin-3 has been reported to regulate the functions of a number of immune cell types. We previously reported that galectin-3 is translocated to immunological synapses in T cells upon T-cell receptor engagement, where it associates with ALG-2-interacting protein X (Alix). Alix is known to coordinate with the endosomal sorting complex required for transport (ESCRT) to promote human immunodeficiency virus (HIV)-1 virion release. We hypothesized that galectin-3 plays a role in HIV-1 viral budding. Cotransfection of cells of the Jurkat T line with galectin-3 and HIV-1 plasmids resulted in increased HIV-1 budding, and suppression of galectin-3 expression by RNAi in Hut78 and primary CD4+ T cells led to reduced HIV-1 budding. We used immunofluorescence microscopy to observe the partial colocalization of galectin-3, Alix and Gag in HIV-1-infected cells. Results from co-immunoprecipitation experiments indicate that galectin-3 expression promotes Alix-Gag p6 association, whereas the results of Alix knockdown suggest that galectin-3 promotes HIV-1 budding through Alix. HIV-1 particles released from galectin-3-expressing cells acquire the galectin-3 protein in an Alix-dependent manner, with proteins primarily residing inside the virions. We also found that the galectin-3 N-terminal domain interacts with the proline-rich region of Alix. Collectively, these results suggest that endogenous galectin-3 facilitates HIV-1 budding by promoting the Alix-Gag p6 association.
原文英語
頁(從 - 到)1022-1035
頁數14
期刊Glycobiology
24
發行號11
DOIs
出版狀態已發佈 - 十一月 1 2014
對外發佈

ASJC Scopus subject areas

  • 生物化學

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