Evaluation and Significance of Cytomegalovirus-Specific Cellular Immune Response in Lung Transplant Recipients

Costa, Cristina; Astegiano, Sara; Terlizzi, Maria Elena; Sidoti, Francesca; Curtoni, Antonio; Solidoro, Paolo; Baldi, S.; Bergallo, Massimiliano; Cavallo, Rossana

doi:10.1016/j.transproceed.2011.03.024

Cited by 30 publications

(25 citation statements)

References 8 publications

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“…T cells may allow prediction of long-term disease susceptibility and may contribute to an improved management of HCMV complications after lung transplantation [156]. Furthermore, the lack of a specific cellular immune response in lung transplantation may lead to the onset of potentially deadly lung disease as evidenced in a patient who developed HCMV pneumonia and eventually died, whereas infectious episodes were favorably resolved in responder patients [157]. Viral replication at non-pathologic levels may not affect the response of T cells as evidenced by the significantly different viral loads in the bronchoalveolar lavage fluid from responders and nonresponders [157].…”

Section: Hcmv Infection In Transplant Recipientsmentioning

confidence: 99%

Human cytomegalovirus infection and atherothrombosis

Popović

Smiljanić

Dobutović

et al. 2011

J Thromb Thrombolysis

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Vascular endothelium, as a key regulator of hemostasis, mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. Endothelial dysfunction caused by acute or chronic inflammation, such as in atherosclerosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites, and at the same time promotes coagulation, thrombin generation, and fibrin deposition in an attempt to close the wound. Life-long persistent infection with human cytomegalovirus (HCMV) has been associated with atherosclerosis. In vivo studies have revealed that HCMV infection of the vessel wall affects various cells including monocytes/macrophages, smooth muscle cells (SMCs) and endothelial cells (ECs). HCMV-infected SMCs within vascular lesions display enhanced proliferation and impaired apoptosis, which contribute to intima-media thickening, plaque formation and restenosis. Monocytes play a central role in the process of viral dissemination, whereas ECs may represent a viral reservoir, maintaining persistent infection in HCMV-infected atherosclerotic patients following the primary infection. Persistent infection leads to dysfunction of ECs and activates proinflammatory signaling involving nuclear factor κB, specificity protein 1, and phosphatidylinositol 3-kinase, as well as expression of platelet-derived growth factor receptor. Activation of these pathways promotes enhanced proliferation and migration of monocytes and SMCs into the intima of the vascular wall as well as lipid accumulation and expansion of the atherosclerotic lesion. Moreover, HCMV infection induces enhanced expression of endothelial adhesion molecules and modifies the proteolytic balance in monocytes and macrophages. As a consequence, infected endothelium recruits naive monocytes from the blood stream, and the concomitant interaction between infected ECs and monocytes enables virus transfer to migrating monocytes. Endothelial damage promotes thrombin generation linking inflammation and coagulation. HCMV, in turn, enhances the thrombin generation. The virus carries on its surface the molecular machinery necessary to initiate thrombin generation, and in addition, may interact with the prothrombinase protein complex thereby facilitating thrombin generation. Thus, infection of endothelium may significantly increase the production of thrombin. This might not only contribute to thrombosis in patients with atherosclerosis, but might also induce thrombin-dependent proinflammatory cell activation. This review summarizes the existing evidence on the role of HCMV in vascular inflammation.

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Section: Hcmv Infection In Transplant Recipientsmentioning

confidence: 99%

Human cytomegalovirus infection and atherothrombosis

Popović

Smiljanić

Dobutović

et al. 2011

J Thromb Thrombolysis

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“…For example, the development of CMV-specific T cell immunity has demonstrated some success in predicting CMV risk (3)(4)(5)(6)(7)(8). It is also widely recognized that across all types of solid organ transplants, the serostatus of both the donor and recipient confer different levels of risk for the development of CMV infection or disease (1,(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Late-Onset Cytomegalovirus (CMV) in Lung Transplant Recipients: Can CMV Serostatus Guide the Duration of Prophylaxis?

Schoeppler

Lyu

Grazia

et al. 2013

American Journal of Transplantation

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Evidence supports the use of 12 months of cytomegalovirus prophylaxis in all at-risk lung transplants; whether cytomegalovirus serostatus can be used to further optimize this duration remains to be determined. The purpose of this retrospective study was to determine if cytomegalovirus serostatus of both donor and recipient were associated with lateonset cytomegalovirus. The primary outcome was the proportion of lung transplants that developed cytomegalovirus infection or disease during the 180-day period following 6 months of prophylaxis in each at-risk serotype. Two hundred forty-four consecutive lung transplants were evaluated, 131 were included.

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“…Despite this uncertainty, a series of intriguing observations has established a compelling association between human herpesvirus infection and IPF. In addition, herpesvirus infection has been linked with chronic allograft rejection and/or fibrosis following solid organ transplants of lung (3), liver (9), and kidney (27). Given the ubiquity of herpesvirus exposure and the relative rarity of IPF, it is unlikely herpesviruses are singular etiologic agents causing this disease.…”

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confidence: 99%