Lytic KSHV infection inhibits host gene expression by accelerating global mRNA turnover
Lytic KSHV infection inhibits host gene expression by accelerating global mRNA turnover
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DOI：
10.1016/s1097-2765(04)00091-7
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发表时间：
2004-03-12
期刊：
影响因子：
16
通讯作者：
Ganem, D
中科院分区：
文献类型：
--
作者：
Glaunsinger, B;Ganem, D
卡波西肉瘤相关疱疹病毒（KSHV）裂解基因产物刺激宿主基因表达已被认为在KS发展中起关键作用。然而，我们发现，裂解KSHV感染强烈抑制宿主基因表达感染早期加速全球mRNA周转。这种功能是由KSHV ORF 37介导的，ORF 37是广泛存在于其他疱疹病毒中的DNA外切核酸酶的同源物，但在KSHV中独特地进化出介导其参与RNA降解的额外功能。KSHV抑制宿主基因表达的能力对KS发病机制模型具有重要意义，KS发病机制模型在裂解感染的细胞中激活宿主转录作为血管生成或致癌因子的来源。
The stimulation of host gene expression by lytic gene products of Kaposi's sarcoma-associated herpesvirus (KSHV) has been proposed to play a critical role in KS development. We show, however, that lytic KSHV infection strongly inhibits host gene expression early in infection by accelerating global mRNA turnover. This function is mediated by KSHV ORF37, a homolog of a DNA exonuclease widely present in other herpesviruses but which in KSHV has uniquely evolved additional functions that mediate its participation in RNA degradation. The ability of KSHV to inhibit host gene expression has important implications for models of KS pathogenesis that invoke activation of host transcription in lytically infected cells as a source of angiogenic or oncogenic factors.