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Review
. 2016 Feb;13(1):10-9.
doi: 10.1007/s11904-016-0297-9.

Partners in Crime: The Role of CMV in Immune Dysregulation and Clinical Outcome During HIV Infection

Michael L Freeman  1 , Michael M Lederman  1 , Sara Gianella  2
Affiliations
Review

Partners in Crime: The Role of CMV in Immune Dysregulation and Clinical Outcome During HIV Infection

Michael L Freeman et al. Curr HIV/AIDS Rep. 2016 Feb.

Abstract

In the current era of combination antiretroviral therapy (ART), human immunodeficiency virus (HIV)-infected individuals are living longer and healthier lives. Nevertheless, HIV-infected persons are at greater risk for age-related disorders, which have been linked to residual immune dysfunction and inflammation. HIV-infected individuals are almost universally co-infected with cytomegalovirus (CMV) and both viruses are associated with inflammation-related morbidities. Therefore, a detailed investigation of the relationship between CMV and aging-related morbidities emerging during chronic HIV infection is warranted. Here, we review the literature on how CMV co-infection affects HIV infection and host immunity and we discuss the gaps in our knowledge that need elucidation.

Keywords: Aging; CMV infection; HIV infection; Immune response; Inflammation.

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Conflict of interest statement

Michael L. Freeman, Michael M. Lederman, and Sara Gianella declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Proposed model connecting CMV, HIV, CD4 T cell dysfunction, and CD8 T cell expansion. We propose a model where HIV infection itself drives inflammation and cytokine production (for example IL-15) promoting CD8+ T cell expansion. HIV infection also induces CD4+ T cell loss and dysfunction, thereby failing to provide help to CD8+ T cells and permitting more CMV replication, which contributes to inflammation and further promotes the expansion of CD8+ T cells. Signals from CMV infection may also promote HIV persistence in CD4+ T cells (dotted line). Expanded CD8+ T cells are unable to control CMV replication, contributing to the vicious cycle. In addition, CD8+ T cell expansion, coupled with a loss of CD4+ T cells (leading to a lower CD4/CD8 T cell ratio) are linked to morbid outcomes of CMV and HIV infections, including cardiovascular risk (and other non AIDS events)
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