Department of Biochemistry, University of Nebraska-Lincoln, Lincoln, NE, United States.
Nebraska Center for Virology, University of Nebraska-Lincoln, Lincoln, NE, United States.
Front Cell Infect Microbiol. 2023 Jun 6;13:1189805. doi: 10.3389/fcimb.2023.1189805. eCollection 2023.
The human betaherpesviruses including human cytomegalovirus (HCMV), human herpesvirus (HHV)-6a and HHV-6b, and HHV-7 infect and establish latency in CD34+ hematopoietic stem and progenitor cells (HPCs). The diverse repertoire of HPCs in humans and the complex interactions between these viruses and host HPCs regulate the viral lifecycle, including latency. Precise manipulation of host and viral factors contribute to preferential maintenance of the viral genome, increased host cell survival, and specific manipulation of the cellular environment including suppression of neighboring cells and immune control. The dynamic control of these processes by the virus regulate inter- and intra-host signals critical to the establishment of chronic infection. Regulation occurs through direct viral protein interactions and cellular signaling, miRNA regulation, and viral mimics of cellular receptors and ligands, all leading to control of cell proliferation, survival, and differentiation. Hematopoietic stem cells have unique biological properties and the tandem control of virus and host make this a unique environment for chronic herpesvirus infection in the bone marrow. This review highlights the elegant complexities of the betaherpesvirus latency and HPC virus-host interactions.
人类β疱疹病毒包括人类巨细胞病毒(HCMV)、人类疱疹病毒(HHV)-6a 和 HHV-6b 以及 HHV-7,感染并潜伏在 CD34+造血干细胞和祖细胞(HPC)中。人类 HPC 的多样性和这些病毒与宿主 HPC 之间的复杂相互作用调节病毒生命周期,包括潜伏。宿主和病毒因素的精确操纵有助于优先维持病毒基因组,增加宿主细胞存活,并对细胞环境进行特定操作,包括抑制邻近细胞和免疫控制。病毒对这些过程的动态控制调节了建立慢性感染所需的细胞间和细胞内信号。这种调节通过直接的病毒蛋白相互作用和细胞信号转导、miRNA 调节以及病毒对细胞受体和配体的模拟来实现,所有这些都导致了细胞增殖、存活和分化的控制。造血干细胞具有独特的生物学特性,病毒和宿主的串联控制使骨髓成为慢性疱疹病毒感染的独特环境。本综述强调了β疱疹病毒潜伏和 HPC 病毒-宿主相互作用的复杂而精妙之处。