阐述宿主细胞调节病毒复制的分子机制利于寻找新的抗病毒靶标。宿主因子Tollip抑制NF-κB激活、负调控IL-1R和TLR信号通路。HIV-1 LTR启动子序列包含NF-κB结合位点，NF-κB通路的调节是调控HIV-1转录的关键。前期工作发现，1）Tollip抑制HIV-1及前病毒DNA的转录；2）干涉Tollip在HIV-1潜伏感染CD4+ T细胞中的表达增强潜伏感染的激活；3）HIV-1可诱导Tollip的表达。因此提出假说：宿主因子Tollip通过阻断NF-κB通路，抑制HIV-1 LTR驱动的转录，调控病毒的复制和潜伏感染。将进一步深入研究：1）Tollip抑制HIV-1转录的分子机制；2）Tollip对HIV-1潜伏感染的调控；3）HIV-1诱导Tollip表达的分子机制。阐明Tollip对HIV-1转录的调节，可揭示HIV-1复制和潜伏感染的调控机制,利于探索抗病毒新策略。

The elucidation of host modulation on viral replication benefits the finding for novel antiviral targets. Host factor Tollip inhibits NF-κB activation and is a negative regulator for IL-R and TLR-mediating signaling. HIV-1 LTR promoter contains the binding sites for NF-κB molecule, and the modulation of NF-κB pathway is the key for regulating viral transcription. Our preliminary data show that, 1)Tollip inhibits transcription of HIV-1 and its proviral DNA;2)The knocking-down of Tollip in HIV-1 latently infected CD4+ T cells promotes viral reactivation from latency; 3) HIV-1 treatment stimulates Tollip expression; So we hypothesize that, Tollip inhibits NF-κB-dependent HIV-1 transcription and maintains viral latency or persistence. We would further study: 1) The molecular mechanisms for Tollip inhibits HIV-1 transcription; 2)the modulation of Tollip on HIV-1 latency; 3) the molecular mechanism for Tollip expression induced by HIV-1 treatment. The elucidation of Tollip modulating HIV-1 transcription would facilitate to uncover the mechanisms of host modulation on HIV-1 replication and persistence, and benefit the development for novel antiviral strategies.