Toll-interacting protein inhibits HIV-1 infection and regulates viral latency

作者：Li, Chuan; Kuang, Wen-Dong; Qu, Di; Wang, Jian-Hua^*

来源：Biochemical and Biophysical Research Communications, 2016, 475(2): 161-168.

DOI：10.1016/j.bbrc.2016.05.065

• HIV-1
• Long-terminal repeat
• Toll-interacting protein
• Viral latency

HIV-1 latency is mainly characterized by a reversible silencing of long-terminal repeat (LTR)-driven transcription of provirus. The existing of repressive factors has been described to contribute to transcription silencing of HIV-1. Toll-interacting protein (Tollip) has been identified as a repressor of Toll like receptors (TLR)-mediated signaling. Our previous study has found that Tollip inhibited NF-kappa B-dependent HIV-1 promoter LTR-driven transcription, indicating the potential role of Tollip in governing viral latency. In this study, by using HIV-1 latently infected Jurkat T-cell and central memory CD4(+) T-cells, we demonstrate the role of Tollip in regulating HIV-1 latency, as the knock-down of Tollip promoted HIV-1 reactivation from both HIV-1 latently infected Jurkat CD4(+) T cells and primary central memory T cells (T-CM). Moreover, we found that the activities of LTR5 derived from multiple HIV-1 subtypes could be repressed by Tollip; Knock-down of Tollip promoted HIV-1 transcription and infection in CD4(+) T cells. Our data indicate a key role of Tollip in suppressing HIV-1 infection and regulating viral latency, which provides a potential host target for combating HIV-1 infection and latency.

• 出版日期2016-6-24
• 单位中国科学院上海巴斯德研究所