Lukac D M, Renne R, Kirshner J R, Ganem D
Howard Hughes Medical Institute and Departments of Microbiology and Medicine, University of California, San Francisco, California, 94143, USA.
Virology. 1998 Dec 20;252(2):304-12. doi: 10.1006/viro.1998.9486.
Kaposi's sarcoma (KS)-associated herpesvirus (KSHV), or human herpesvirus 8, is a lymphotropic virus strongly linked to several AIDS-related neoplasms. The primary reservoir of infection consists of latently infected B lymphocytes and possibly other mononuclear cells. Viral reactivation from latency and spread from this lymphoid reservoir is presumably required for development of nonlymphoid tumors like KS. Here we show that deregulated expression of a single viral gene, ORF 50, which encodes a transactivator able to selectively upregulate delayed-early viral genes, suffices to disrupt latency and induce the lytic gene cascade in latently infected B cells. The identification of this gene opens the way to studies of the physiologic mechanisms controlling reactvation of KSHV from latency.
卡波西肉瘤相关疱疹病毒（KSHV），即人类疱疹病毒8型，是一种与多种艾滋病相关肿瘤密切相关的嗜淋巴细胞病毒。感染的主要储存库由潜伏感染的B淋巴细胞以及可能的其他单核细胞组成。非淋巴样肿瘤（如卡波西肉瘤）的发生可能需要病毒从潜伏状态重新激活并从这个淋巴样储存库中传播。在这里，我们表明，单个病毒基因ORF 50的表达失调就足以破坏潜伏状态并在潜伏感染的B细胞中诱导裂解基因级联反应，该基因编码一种能够选择性上调延迟早期病毒基因的反式激活因子。该基因的鉴定为研究控制KSHV从潜伏状态重新激活的生理机制开辟了道路。
