HCMV reprogramming of infected monocyte survival and differentiation: a Goldilocks phenomenon

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 mono...

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Bibliographic Details
Published in:Viruses 2014-02, Vol.6 (2), p.782-807
Main Authors: Stevenson, Emily V, Collins-McMillen, Donna, Kim, Jung Heon, Cieply, Stephen J, Bentz, Gretchen L, Yurochko, Andrew D
Format: Article
Language:English
Subjects:
Cell Differentiation
Cell Survival
Cytomegalovirus - physiology
HCMV
Host-Pathogen Interactions
Human cytomegalovirus
Humans
macrophage
Macrophages - physiology
Macrophages - virology
monocyte
Monocytes - physiology
Monocytes - virology
polarization
receptor-ligand
Review
signaling
survival
viral dissemination
viral persistence
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Summary: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.
ISSN:1999-4915
1999-4915
DOI:10.3390/v6020782