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HCMV Reprogramming of Infected Monocyte Survival and Differentiation: A Goldilocks Phenomenon

机译：HCMV重编程感染单核细胞的生存和分化：金发姑娘现象。

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The wide range of disease pathologies seen in multiple organ sites associated with human cytomegalovirus (HCMV) infection results from the systemic hematogenous dissemination of the virus, which is mediated predominately by infected monocytes. In addition to their role in viral spread, infected monocytes are also known to play a key role in viral latency and life-long persistence. However, in order to utilize infected monocytes for viral spread and persistence, HCMV must overcome a number of monocyte biological hurdles, including their naturally short lifespan and their inability to support viral gene expression and replication. Our laboratory has shown that HCMV is able to manipulate the biology of infected monocytes in order to overcome these biological hurdles by inducing the survival and differentiation of infected monocytes into long-lived macrophages capable of supporting viral gene expression and replication. In this current review, we describe the unique aspects of how HCMV promotes monocyte survival and differentiation by inducing a “finely-tuned” macrophage cell type following infection. Specifically, we describe the induction of a uniquely polarized macrophage subset from infected monocytes, which we argue is the ideal cellular environment for the initiation of viral gene expression and replication and, ultimately, viral spread and persistence within the infected host.
机译：在与人类巨细胞病毒（HCMV）感染相关的多个器官部位中看到的广泛的疾病病理是由于病毒的系统性血源性传播引起的，这种疾病主要由被感染的单核细胞介导。除了它们在病毒传播中的作用外，感染的单核细胞在病毒潜伏期和终生持久性中也起着关键作用。但是，为了利用受感染的单核细胞进行病毒扩散和持久性，HCMV必须克服许多单核细胞生物学障碍，包括其自然寿命短以及无法支持病毒基因表达和复制。我们的实验室表明，HCMV能够通过诱导被感染的单核细胞存活和分化为能够支持病毒基因表达和复制的长寿巨噬细胞，从而操纵被感染的单核细胞的生物学从而克服这些生物学障碍。在当前的综述中，我们描述了HCMV如何通过在感染后诱导“微调”的巨噬细胞类型来促进单核细胞存活和分化的独特方面。具体来说，我们描述了从受感染的单核细胞诱导的独特极化的巨噬细胞亚群的诱导，我们认为这是启动病毒基因表达和复制以及最终在受感染宿主内进行病毒扩散和持久性的理想细胞环境。

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