Infections Transmitted by Transplantation

Morris, Michele; Fischer, Staci A.; Ison, Michael G.

doi:10.1016/j.idc.2010.02.002

Cited by 50 publications

(31 citation statements)

References 71 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, in immunocompromised individuals such as patients receiving immunosupressive therapy due to organ transplantation, HCMV infection accounts for a high morbidity and mortality rate. In addition, transplant organ rejection is highly increased in infected patients [18,[21][22][23].…”

Section: Hcmv Infection In Transplant Recipientsmentioning

confidence: 99%

“…In neonates primary HCMV infection may cause life-threatening diseases and it may be associated with several neurological birth defects [17]. Whereas in healthy, immunocompetent individuals, HCMV infection remains mainly asymptomatic, persistent or recurrent infection of immunocompromised individuals such as acquired immune deficiency syndrome patients [18,19] or transplant organ recipients may result in significant morbidity and mortality [20][21][22][23]. Chronic infection of the vasculature with HCMV has been linked to the development of cardiovascular diseases such as atherosclerosis, restenosis, and transplant vascular sclerosis [24][25][26][27].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Human cytomegalovirus infection and atherothrombosis

Popovic

Smiljanić

Dobutovic

et al. 2011

J Thromb Thrombolysis

View full text Add to dashboard Cite

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.

show abstract

Section: Hcmv Infection In Transplant Recipientsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Human cytomegalovirus infection and atherothrombosis

Popovic

Smiljanić

Dobutovic

et al. 2011

J Thromb Thrombolysis

View full text Add to dashboard Cite

show abstract

“…Some of these infections, which might be detected by donor and recipient screening, involve infection from a seropositive donor to a seronegative recipient, including the transmission of cytomegalovirus (CMV), Epstein-Barr virus (EBV), or toxoplasmosis, while others are unexpected despite routine donor screening. Unexpected clusters of donor-derived viral infections in transplant recipients have occurred, including rabies, West Nile virus (WNV), Human immunodeficiency virus (HIV), herpes simplex virus, hepatitis B virus (HBV), and hepatitis C virus (HCV) (Morris et al, 2010). Nosocomial donor infections are most commonly related to bacterial pathogens.…”

Section: Potential Infections Of the Donormentioning

confidence: 99%

Donor-Derived Infectious Complications and Disease Transmission

Chan¹,

Lee²

2012

Liver Transplantation - Technical Issues and Complications

View full text Add to dashboard Cite

“…Additionally, there are areas of the United States that do not have access to timely nucleic acid testing to screen for transmissible viruses. Although transplant transmitted infections are uncommon, they continue to occur due to recognized challenges in detecting these infections and the use of imperfect screening tools (3)(4)(5). Even if a donor transmitted infection is suspected in a transplant recipient, clinicians may be unaware of how to obtain and/or report relevant donor/recipient information (6).…”

Section: Introductionmentioning

confidence: 99%