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Review
. 2007 Oct;19(5):577-82.
doi: 10.1016/j.coi.2007.07.012. Epub 2007 Aug 22.

Acceleration of allograft failure by cytomegalovirus

Daniel N Streblow  1 , Susan L Orloff, Jay A Nelson
Affiliations
Review

Acceleration of allograft failure by cytomegalovirus

Daniel N Streblow et al. Curr Opin Immunol. 2007 Oct.

Abstract

A number of human herpesviruses are important opportunistic pathogens that have been associated with increased morbidity and mortality in transplant recipients including human cytomegalovirus (HCMV), HHV6, HHV7, HHV8 as well as HSV-1, VZV. However, HCMV has been linked both epidemiologically and through the use of animal models to the acceleration of acute and chronic allograft rejection. This review will cover the pathophysiology, epidemiology, and mechanisms of CMV-associated disease in the setting of transplantation.

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Conflict of interest statement

Conflicts of Interest:

No conflicts of interest are declared by the authors.

Figures

Figure 1
Figure 1. Role of Cytomegalovirus Accelerated Chronic Allograft Rejection
In chronically infected human SOT recipients, CMV reactivates from latently infected monocytes or endothelial cells (EC) in the presence of the inflammatory alloreactive environment of the allograft. EC injury is an important first step in the development of vascular disease associated with CR. The response to injury involves the local release of growth factors, chemokines, and cytokines, as well as the up-regulation of adhesion molecules on the EC, which together promote monocyte/macrophage migration and platelet adherence to the injured site. Wound repair and angiogenesis processes drive SMC migration and proliferation in the affected blood vessels, which leads to eventual vessel narrowing, occlusion, and graft failure due to ischemia.
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