Cytomegalovirus infection and viral‐induced transformation of human endothelial cells

Smiley, M. Lynn; Mar, Eng-Chun; Huang, Eng‐Shang

doi:10.1002/jmv.1890250212

Cited by 81 publications

(43 citation statements)

References 51 publications

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“…CMV is capable of infecting components of the vascular wall, in particular, endothelial cells (34)(35)(36) and smooth muscle cells (37). Like all other herpesviruses, CMV is able to turn into the latent state after acute infection.…”

Section: Discussionmentioning

confidence: 99%

Cytomegalovirus infection enhances smooth muscle cell proliferation and intimal thickening of rat aortic allografts.

Lemström¹,

Bruning²,

Bruggeman³

et al. 1993

J. Clin. Invest.

131

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Inbred DA (AG-B4, RT1 a) and WF (AG-B2, RT1') rats were used as donors and recipients of aortic allografts. The recipient rats were inoculated i.p. either on day 1 (early infection) or on day 60 (late infection) with iOs plaque-forming units of rat cytomegalovirus (RCMV). The control rats were left noninfected. The presence of viral infection was demonstrated by plaque assays from biopsies of the salivary glands, liver, and spleen at sacrifice. The rats received 300 gCi 13H Ithymidine by i.v. injection 3 h before sacrifice, and the grafts were removed at various time points for histology, immunohistochemistry, and autoradiography. RCMV infection significantly enhanced the generation of allograft arteriosclerosis. Infection at the time of transplantation had two important effects. First, the infection was associated with an early, prominent inflammatory episode and proliferation of inflammatory cells in the allograft adventitia. Second, the viral infection doubled the proliferation rate of smooth muscle cells and the arteriosclerotic alterations in the intima. In late infection the impact of RCMV infection on the allograft histology was nearly nonexistent. RCMV infection showed no effect in syngeneic grafts. These results suggest that early infection is more important to the generation of accelerated allograft arteriosclerosis than late infection, and that an acute alloimmune response must be associated with virus infection, to induce accelerated allograft arteriosclerosis. RCMVinfected aortic allografts, as described here, provide the first experimental model to investigate the interaction between the virus and the vascular wall of the transplant. (J. Clin. Invest. 1993. 92:549-558.)

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Section: Discussionmentioning

confidence: 99%

Cytomegalovirus infection enhances smooth muscle cell proliferation and intimal thickening of rat aortic allografts.

Lemström¹,

Bruning²,

Bruggeman³

et al. 1993

J. Clin. Invest.

131

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“…In the United States, the incidence of positive serology for cytomegalovirus is 60 to 70% of the population 27 ; in Brazil, it reaches more than 90% 28 . The mechanism by which cytomegalovirus may lead to atherosclerosis has not been well established; however, it is believed to stimulate the proliferation of smooth muscle cells and to cause procoagulant changes in the endothelium, contributing to the formation of atherosclerotic plaque 29 . The first report on the association of cytomegalovirus and allograft vasculopathy was by Grattan et al 30 at Stanford University.…”

mentioning

confidence: 99%

Analysis of the risk factors for allograft vasculopathy in asymptomatic patients after cardiac transplantation

Bacal¹,

Veiga²,

Fiorelli³

et al. 2000

Arq. Bras. Cardiol.

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“…Alternatively, virion US28 may modify cell tropism by binding to cell surface proteins such as fractalkine, thereby facilitating viral absorption and entry. Cytokine-activated endothelial cells have been shown to support viral replication (38,51), and surface expression of fractalkine in these cells is also up regulated in response to cytokines (12). Binding of plasma-borne virions or infected cells to fractalkine on activated endothelial cells lining the vasculature may play a role in dissemination from initial sites of mucosal infection and provide a molecular basis for observations of CMV's role in cardiovascular disease (8,43) and transplant-related vascular disease (9).…”

Section: Discussionmentioning

confidence: 99%

Characterization of the Rhesus Cytomegalovirus US28 Locus

Penfold

Schmidt

Dairaghi

et al. 2003

J Virol

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Human cytomegalovirus (CMV) US28 (and the related open reading frame [ORF] US27) are G-proteincoupled receptor homologs believed to play a role in viral pathogenesis. In vitro, US28 has been shown to bind and internalize ligands, as well as activate intracellular signaling in response to certain chemokines, and to initiate the migration of smooth muscle cells to chemokine gradients. To assess the role of US28 in vivo, we examined the rhesus model and sequenced and characterized the rhesus CMV US28 locus. We found that rhesus CMV carries five tandem homologs of US28, all widely divergent from US28 and from each other. By reverse transcription-PCR and Northern analysis, we demonstrated expression of these ORFs in infected cells. With stable cell lines expressing these ORFs, we analyzed the homolog's binding and signaling characteristics across a wide range of chemokines and found one (RhUS28.5) to have a ligand binding profile similar to that of US28. In addition, we localized US28 and the rhesus CMV homolog RhUS28.5 to the envelope of infectious virions, suggesting a role in viral entry or cell tropism.

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Cytomegalovirus infection and viral‐induced transformation of human endothelial cells

Cited by 81 publications

References 51 publications

Cytomegalovirus infection enhances smooth muscle cell proliferation and intimal thickening of rat aortic allografts.

Cytomegalovirus infection enhances smooth muscle cell proliferation and intimal thickening of rat aortic allografts.

Analysis of the risk factors for allograft vasculopathy in asymptomatic patients after cardiac transplantation

Characterization of the Rhesus Cytomegalovirus US28 Locus

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