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病毒和宿主网络分析的人类细胞巨型病毒转录组在延迟状态

Donna Collins-McMillen^1,2, Diogo De Oliveira Pessoa³, Kristen Zarrella²

¹BIO5 Institute, University of Arizona, Tucson, Arizona, United States of America.

bioRxiv : the preprint server for biology

|June 3, 2024

概括

人类细胞巨乳病毒 (HCMV) 基因UL135和UL138对逆调节病毒延迟和重新激活. 它们的缺失影响病毒基因表达和宿主细胞分化,揭示了新的调节作用.

科学领域:

病毒学病毒学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

人类细胞巨乳病毒 (HCMV) 导致终身感染,常常保持潜伏状态.
了解HCMV的潜伏和再激活对于管理感染至关重要,特别是在免疫受损的个体中.
特定的病毒基因,如UL135和UL138,参与调节宿主细胞内的HCMV生命周期.

研究的目的:

研究HCMV基因UL135和UL138在调节病毒延迟和重新激活方面的对立作用.
为了比较CD34+人类原生细胞 (HPC) 中的UL135和UL138和没有UL135和UL138的HCMV感染的转录特征.
确定潜在地协调ULb'基因与pUL135.5的表达的宿主转录因子.

主要方法:

利用THP-1细胞系作为HCMV延迟和重新激活的模型.
进行RNA测序以比较HCMV感染细胞与UL135和UL138.8感染细胞之间的转录特征.
进行了转录网络分析,以确定与病毒基因相互作用的宿主因素.

主要成果:

失去UL138导致病毒基因表达增加,并增强了支持病毒复制的细胞的分化.
丢失UL135导致在延迟建立期间初始病毒基因表达减少.
缺少UL135阻止了11个ULb'区域病毒基因的表达,即使在重新激活刺激后.

结论:

HCMV UL135和UL138在控制潜伏和重新激活期间的病毒基因表达方面发挥着关键的,对立的作用.
这些病毒基因可能会影响造血细胞分化过程.
UL135似乎对ULb'区域内特定病毒基因的表达至关重要,可能通过与宿主转录因子的协调.

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