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HCMV Infection and Apoptosis: How Do Monocytes Survive HCMV Infection?

1
BIO5 Institute, Department of Immunology, University of Arizona, Tucson, AZ 85721, USA
2
Department of Microbiology & Immunology, Center for Molecular & Tumor Virology, Louisiana State University Health Sciences Center—Shreveport, Shreveport, LA 71130, USA
3
Center for Cardiovascular Diseases & Sciences, Louisiana State University Health Sciences Center—Shreveport, Shreveport, LA 71130, USA
4
Feist-Weiller Cancer Center, Louisiana State University Health Sciences Center—Shreveport, Shreveport, LA 71130, USA
5
Center of Excellence in Arthritis & Rheumatology, Louisiana State University Health Sciences Center—Shreveport, Shreveport, LA 71130, USA
*
Author to whom correspondence should be addressed.
Viruses 2018, 10(10), 533; https://doi.org/10.3390/v10100533
Received: 8 August 2018 / Revised: 10 September 2018 / Accepted: 26 September 2018 / Published: 29 September 2018
(This article belongs to the Special Issue Recent Advances in Cytomegalovirus Research)
Human cytomegalovirus (HCMV) infection of peripheral blood monocytes plays a key role in the hematogenous dissemination of the virus to multiple organ systems following primary infection or reactivation of latent virus in the bone marrow. Monocytes have a short life span of 1–3 days in circulation; thus, HCMV must alter their survival and differentiation to utilize these cells and their differentiated counterparts—macrophages—for dissemination and long term viral persistence. Because monocytes are not initially permissive for viral gene expression and replication, HCMV must control host-derived factors early during infection to prevent apoptosis or programmed cell death prior to viral induced differentiation into naturally long-lived macrophages. This review provides a short overview of HCMV infection of monocytes and describes how HCMV has evolved to utilize host cell anti-apoptotic pathways to allow infected monocytes to bridge the 48–72 h viability gate so that differentiation into a long term stable mature cell can occur. Because viral gene expression is delayed in monocytes following initial infection and only occurs (begins around two to three weeks post infection in our model) following what appears to be complete differentiation into mature macrophages or dendritic cells, or both; virally-encoded anti-apoptotic gene products cannot initially control long term infected cell survival. Anti-apoptotic viral genes are discussed in the second section of this review and we argue they would play an important role in long term macrophage or dendritic cell survival following infection-induced differentiation. View Full-Text
Keywords: human cytomegalovirus; apoptosis; programmed cell death; cell signaling; monocytes; macrophages; survival; differentiation human cytomegalovirus; apoptosis; programmed cell death; cell signaling; monocytes; macrophages; survival; differentiation
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Collins-McMillen, D.; Chesnokova, L.; Lee, B.-J.; Fulkerson, H.L.; Brooks, R.; Mosher, B.S.; Yurochko, A.D. HCMV Infection and Apoptosis: How Do Monocytes Survive HCMV Infection? Viruses 2018, 10, 533.

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