Atherosclerosis induced by infection with Marek’s disease herpesvirus in chickens

Fabricant, Catherine G.; Fabricant, J.

doi:10.1016/s0002-8703(99)70276-0

Cited by 74 publications

(50 citation statements)

References 7 publications

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“…The accelerating effect of herpes virus on atherosclerosis was initially noted with Marek disease virus (MDV) in chickens, and subsequently confirmed by the observation that the virus induced atherosclerosis even in normocholesterolemic chickens (6). In the CMV-infected BALB/c mouse, viral antigens were demonstrable in aortic endothelial and smooth muscle cells, accompanied by inflammatory cells typically seen in atherosclerotic lesions (7), suggesting an inflammatory response induced by the virus.…”

Section: Animal Modelsmentioning

confidence: 90%

“…Of all evaluated pathogens, only IgG seropositivity to HSV-2 (p = 0.05) and IgA seropositivity to EBV (p = 0.001) as well as H. pylori (p = 0.002) revealed an independent significant association with future cardiovascular death. However, when infectious burden was evaluated, patients seropositive to > 5 pathogens compared with those seropositive to <4 pathogens had a 5.1 (1,(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18) higher risk of future cardiac death. This result was mainly driven by the pathogen burden of seropositivities to Herpes viridae (p < 0.0001).…”

Section: Total Pathogen Burdenmentioning

confidence: 99%

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The Role of Viruses in Cardiac Allograft Vasculopathy

Valantine

2004

American Journal of Transplantation

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Considerable evidence suggests a role for viruses in transplant arteriosclerosis (TA), including observational data, experimental models and therapeutic trials implicating human cytomegalovirus (HCMV) in the progression to TA. In pediatric heart transplant patients, adenoviral genome in endomyocardial biopsies (EMB) is an important predictor of TA and graft loss. During CMV viremia, EMBs from adult patients demonstrate endothelialitis and vascular smooth muscle cell proliferation. These changes are predictors of subsequent diffuse TA. HCMV immediate early proteins (IE-1 and IE-2) increase the constitutive expression of intercellular adhesion molecule-1 (ICAM-1) independent of other intracellular cytokines. Likewise, viral chemokines such as US28 have been implicated in vascular disease because of their ability to induce smooth muscle cell migration. Recent data suggests that CMV might accelerate TA through its ability to abrogate the vascular protective effects of the endothelium-derived nitric oxide system (eNOS). Confirmation of causality requires clinical trials demonstrating that antiviral agents such as ganciclovir inhibit TA. Such studies in patients though limited to retrospective analyses, suggest that ganciclovir prophylaxis early after heart transplantation reduces the risk of TA. These observations emphasize the need for randomized controlled clinical trials to confirm a causal role for CMV (and other viruses) in TA.

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Section: Animal Modelsmentioning

confidence: 90%

Section: Total Pathogen Burdenmentioning

confidence: 99%

The Role of Viruses in Cardiac Allograft Vasculopathy

Valantine

2004

American Journal of Transplantation

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“…Oku et al [92] suggested that phenotype transformation of intimal cell migrating from the tunica media to play an important role in the initiation and the development of atherosclerosis. Casale et al [100] studied the cellular events of quail atherosclerosis using monoclonal antibodies to alpha-actin and chicken macrophages and effectively identified the presence of SMC and macrophages, respectively, as constituents of the atherosclerotic lesions. The presence of macrophage, as well as SMC proliferation, was ob-served in early lesions.…”

Section: Birdsmentioning

confidence: 99%

Vascular Smooth Muscle Cells and the Comparative Pathology of Atherosclerosis

Al-Sadi¹

2012

Current Basic and Pathological Approaches to the Function of Muscle Cells and Tissues - From Molecules to Humans

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“…31,32 Moreover, a related herpesvirus known as Marek's disease virus (MDV) was found to cause the formation of atherosclerotic lesions in the aortas of chickens and led to accumulation of cholesterol in the aortic wall of MDV-infected chickens. 33 There is currently no vaccine available against HCMV 251 and benefits of treatment with available drugs-foscarnet, gancyclovir and cidofovir-are undermined by toxicity and emergence of drug-resistant strains [34][35][36][37] indicating the need for additional therapeutic approaches. The serious medical problems associated with HCMV infection have thus stimulated research aimed at understanding the complex interplay of viral and host functions that lead to pathogenesis.…”

mentioning

confidence: 99%

Genetic control of innate immune responses against cytomegalovirus: MCMV meets its match

2002

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Cytomegalovirus (CMV) is a widespread pathogen that is All Ly49 receptors characterized to date interact with MHC class I molecules on potential target cells, resulting in the accumulation of signals to the NK to either 'kill' or 'ignore' the cell based upon the repertoire of MHC class I molecules expressed. The identification of Cmv1 as Ly49H, a stimulatory member of the Ly49 family, adds an interesting twist to the Ly49 story. Although the ligand of Ly49H is not yet known, there is already compelling evidence that the ligand is upregulated on virally infected cells, resulting in specific activation of Ly49H-expressing NK cells. This review provides an historical perspective of the MCMV infection model from its inception to the discovery of the gene responsible for the phenotype and provides a basis for further experiments aimed at understanding the role of NK cells, in general, and Ly49H, in particular, in mediating resistance to cytomegalovirus.

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Atherosclerosis induced by infection with Marek’s disease herpesvirus in chickens

Cited by 74 publications

References 7 publications

The Role of Viruses in Cardiac Allograft Vasculopathy

The Role of Viruses in Cardiac Allograft Vasculopathy

Vascular Smooth Muscle Cells and the Comparative Pathology of Atherosclerosis

Genetic control of innate immune responses against cytomegalovirus: MCMV meets its match

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