Kaposi's sarcoma-associated herpesvirus and innate immunity.
Kaposi's sarcoma-associated herpesvirus and innate immunity.
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DOI：
10.2217/fvl.10.5
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发表时间：
2010-03-01
期刊：
影响因子：
3.1
通讯作者：
Damania B
中科院分区：
文献类型：
--
作者：
West JA;Damania B
卡波西肉瘤相关疱疹病毒（Kaposi's sarcoma-associated herpesvirus，KSHV）是最近发现的人类疱疹病毒，于1994年首次从卡波西肉瘤病变中分离和鉴定。它是卡波西肉瘤的病原体，卡波西肉瘤是一种血管病变，是艾滋病患者中的主要癌症。KSHV也是两种B细胞淋巴瘤，原发性渗出性淋巴瘤和多中心Castleman病的主要病原体。KSHV可以存在于裂解期，其中病毒DNA被活跃地复制并且病毒粒子被组装，或者存在于潜伏期，其中病毒基因组通过蛋白质-蛋白质相互作用被束缚到宿主染色体。裂解周期通常发生在初次感染后，在大多数细胞类型中，在72-96小时内，病毒进入潜伏状态。潜伏期的再激活也导致裂解周期的启动，这是病毒在宿主中繁殖和存活所必需的。几种KSHV蛋白已经涉及调节宿主对病毒感染的免疫应答。本文总结了最近的发现涉及先天免疫反应KSHV感染。
Kaposi's sarcoma-associated herpesvirus (KSHV) is the most recently discovered human herpesvirus, first isolated and identified from a Kaposi's sarcoma lesion in 1994. It is the etiological agent of Kaposi's sarcoma, a vascular lesion that is the predominant cancer among AIDS patients. KSHV is also the primary etiological agent of two B-cell lymphomas, primary effusion lymphoma and multicentric Castleman's disease. KSHV can exist in either a lytic phase, in which the viral DNA is actively replicated and virions are assembled, or in a latent phase, in which the viral genome is tethered to the host chromosome via protein–protein interactions. The lytic cycle generally occurs following primary infection, and within 72–96 h in most cell types, the virus enters the latent state. Reactivation from latency also leads to the intiation of the lytic cycle, which is necessary for virus propagation and survival in the host. Several KSHV proteins have been implicated in modulation of the host immune response to viral infection. This article summarizes recent discoveries involving the innate immune response to KSHV infection.
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