Latent viral infection is and will be the bottleneck for virus eradications. Recent studies on viral-host interaction have emphasized on latency reduction by the activated anti-viral immune responses, however the role played by the regulatory immune responses immune system during the latency establishment has not been fully investigated. In this study, we will test the scientific questions if the regulatory T (Treg) cells, the major player for the regulatory immune responses, could contribute and play an important role in the establishment of HSV1 latent infection and its reactivation. With a HSV1 ocular infection as a murine model, we will employ HSV1 ocular infection, Treg tracing, knockout, replacing back, and stress model to investigate if Treg cells are strongly correlated to the HSV1 lytic infection, and are absolutely required for the establishment of its latency. Under suppression of host immune responses under the stressed condition, we will study Treg cell play also a major role to help to reactivate HSV1 out of the latent infection. Therefore, our study could provide the evidences to show the importance of Treg cells during the establishing latency and reactivating from the latency for HSV1 infection. With that, we could design a better antiviral strategy against HSV1.
HSV病毒的潜伏感染(Latent infection)是目前和未来临床防治的难题。近年来,潜伏感染相关的免疫调控机制成为研究热点,抗病毒免疫反应对潜伏控制作用已经报道,但抑制型免疫反应的作用极少报道。本研究将针对调节性T细胞(Treg)在抑制抗病毒CD8+T细胞过程中,为HSV1建立潜伏感染和复活(Reactivation)中起到重要的作用展开研究。通过HSV1眼部感染模型、stress束缚模型、Treg细胞示踪技术、Treg细胞敲除及回补等实验,研究其与HSV1的感染过程密切相关性,且为HSV1建立潜伏感染所必需;进一步探明在免疫低下情况下,Treg细胞通过消弱抗HSV1细胞免疫反应使HSV1从潜伏感染中再激活的证据。因此,Treg细胞可能成为阻断HSV1病毒裂解感染进入潜伏感染的切入点,为打破病毒生活周期,彻底清除病毒提供借鉴。
HSV病毒的潜伏感染(Latent infection)是目前和未来临床防治的难题。近年来,潜伏感染相关的免疫调控机制成为研究热点,抗病毒免疫反应对潜伏控制作用已经报道,但抑制型免疫反应的作用极少报道。本研究将针对调节性T细胞(Treg)在抑制抗病毒CD8+T细胞过程中,为HSV1建立潜伏感染和复活(Reactivation)中起到重要的作用展开研究。通过HSV1眼部感染模型、stress束缚模型、Treg细胞示踪技术、Treg细胞敲除及回补等实验,研究其与HSV1的感染过程密切相关性,且为HSV1建立潜伏感染所必需;进一步探明在免疫低下情况下,Treg细胞通过消弱抗HSV1细胞免疫反应使HSV1从潜伏感染中再激活的证据。因此,Treg细胞可能成为阻断HSV1病毒裂解感染进入潜伏感染的切入点,为打破病毒生活周期,彻底清除病毒提供借鉴。
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数据更新时间:2023-05-31
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