The human T cell leukemia virus persists in vivo in 103 to 106 clones of T lymphocytes that appear to survive for the lifetime of the host. The plus strand of the provirus is typically transcriptionally silent in freshly isolated lymphocytes, but the strong, persistently activated cytotoxic T lymphocyte (CTL) response to the viral antigens indicates that the virus is not constantly latent in vivo. There is now evidence that the plus strand is transcribed in intense intermittent bursts that are triggered by cellular stress, modulated by hypoxia and glycolysis, and inhibited by polycomb repressive complex 1 (PRC1). The minus-strand gene hbz is transcribed at a lower, more constant level but is silent in a proportion of infected cells at a given time. Viral genes in the sense and antisense strands of the provirus play different respective roles in latency and de novo infection: Expression of the plus-strand gene tax is essential for de novo infection, whereas hbz appears to facilitate survival of the infected T cell clone in vivo.

中文翻译：

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人类 T 细胞白血病病毒 HTLV-1 潜伏期的调节。

人类 T 细胞白血病病毒在体内持续存在于 103 至 106 个 T 淋巴细胞克隆中，这些 T 淋巴细胞克隆似乎可以在宿主的一生中存活。原病毒的正链在新分离的淋巴细胞中通常是转录沉默的，但对病毒抗原的强烈、持续激活的细胞毒性 T 淋巴细胞 (CTL) 反应表明病毒在体内并非一直潜伏。现在有证据表明，正链在强烈的间歇爆发中转录，这些爆发由细胞应激触发，由缺氧和糖酵解调节，并被多梳抑制复合物 1 (PRC1) 抑制。负链基因 hbz 以较低、更稳定的水平转录，但在给定时间在一定比例的感染细胞中是沉默的。