Collins-McMillen Donna, De Oliveira Pessoa Diogo, Zarrella Kristen, Parkins Christopher J, Daily Michael, Moorman Nathaniel J, Kamil Jeremy P, Caposio Patrizia, Padi Megha, Goodrum Felicia D
BIO5 Institute, University of Arizona, Tucson, Arizona, United States of America.
Department of Immunobiology, University of Arizona, Tucson, Arizona, United States of America.
bioRxiv. 2024 May 21:2024.05.21.594597. doi: 10.1101/2024.05.21.594597.
HCMV genes and play opposing roles regulating latency and reactivation in CD34 human progenitor cells (HPCs). Using the THP-1 cell line model for latency and reactivation, we designed an RNA sequencing study to compare the transcriptional profile of HCMV infection in the presence and absence of these genes. The loss of results in elevated levels of viral gene expression and increased differentiation of cell populations that support HCMV gene expression and genome synthesis. The loss of results in diminished viral gene expression during an initial burst that occurs as latency is established and no expression of eleven viral genes from the UL' region even following stimulation for differentiation and reactivation. Transcriptional network analysis revealed host transcription factors with potential to regulate the UL' genes in coordination with pUL135. These results reveal roles for and in regulation of viral gene expression and potentially hematopoietic differentiation.
人巨细胞病毒（HCMV）基因在调节CD34人祖细胞（HPCs）的潜伏和再激活过程中发挥着相反的作用。利用THP-1细胞系模型进行潜伏和再激活研究，我们设计了一项RNA测序研究，以比较在有或没有这些基因的情况下HCMV感染的转录谱。[基因名称1]的缺失导致病毒基因表达水平升高，以及支持HCMV基因表达和基因组合成的细胞群体分化增加。[基因名称2]的缺失导致在建立潜伏时出现的初始爆发期间病毒基因表达减少，并且即使在刺激分化和再激活后，UL'区域的11个病毒基因也没有表达。转录网络分析揭示了有可能与pUL135协同调节UL'基因的宿主转录因子。这些结果揭示了[基因名称1]和[基因名称2]在调节病毒基因表达以及潜在的造血分化中的作用。
