HCMV reprogramming of infected monocyte survival and differentiation: A goldilocks phenomenon

65Citations
Citations of this article
87Readers
Mendeley users who have this article in their library.

Abstract

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{norm of matrix} 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. © 2014 by the authors; licensee MDPI, Basel, Switzerland.

Cite

CITATION STYLE

APA

Stevenson, E. V., Collins-McMillen, D., Kim, J. H., Cieply, S. J., Bentz, G. L., & Yurochko, A. D. (2014, February 13). HCMV reprogramming of infected monocyte survival and differentiation: A goldilocks phenomenon. Viruses. MDPI AG. https://doi.org/10.3390/v6020782

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free