Virus-induced atherosclerosis.

Fabricant, Catherine G.; Fabricant, J.; Litrenta, M M; Minick, C R

doi:10.1084/jem.148.1.335

Cited by 444 publications

(203 citation statements)

References 9 publications

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“…The ubiquity and the ability to cycle between dormancy and replication make HHVs candidates for the role of constant triggers of immunoactivation that is closely related to the development of atherosclerosis. Early in 1980s, it was shown in chickens infected with Marek disease herpesvirus12 that diet‐induced experimental atherosclerosis developed at a higher rate than in control animals. Evidence of the involvement of HHVs in the development of atherosclerosis and restenosis after coronary angioplasty and in the acceleration of atherosclerosis development in heart transplant recipients has also been reported 29.…”

Section: Discussionmentioning

confidence: 99%

“…Among known human viruses, human herpesviruses (HHVs) fit these criteria. Studies in animal models have demonstrated that HHVs are capable of contributing to the development of atherosclerosis‐type pathologies 12. Data on the involvement of HHVs in human atherosclerosis are far less conclusive13 and are predominantly based on epidemiological studies.…”

Section: Introductionmentioning

confidence: 99%

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Cytomegalovirus‐Productive Infection Is Associated With Acute Coronary Syndrome

Nikitskaya

Lebedeva

Ivanova

et al. 2016

JAHA

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BackgroundAlthough an association between human herpesvirus (HHV) infection and atherosclerosis has been suggested, the data supporting such an association are controversial and, in most cases, are based on serological evidence or on the presence of cell‐associated HHV DNA, which do not report about actual viral replication. We quantified the DNA of all 8 types of HHVs in plasma, in which their presence is evidence of viral replication.Methods and ResultsUsing quantitative real‐time polymerase chain reaction, we evaluated the presence of HHV DNA in blood samples obtained at the time of hospitalization from 71 patients with acute coronary syndrome, 26 patients with stable coronary artery disease, and 53 healthy volunteers and in atherosclerotic plaques of 22 patients with peripheral artery disease who underwent endarterectomy. HHV‐5 (cytomegalovirus [CMV]) was the only HHV with a level that was higher in acute coronary syndrome patients than in the control group and that correlated with the level of high‐sensitivity C‐reactive protein. The numbers of effector memory T cells positively correlated with the numbers of CMV genome copies in carotid arteries plaques, whereas the numbers of central memory T cells negatively correlated with CMV copy numbers.ConclusionsOf all HHV levels, only CMV was higher in patients with stable coronary artery disease and acute coronary syndrome than in the healthy group, and its load correlated with the level of high‐sensitivity C‐reactive protein. The level of CMV in atherosclerotic plaques correlated with the state of immunoactivation of lymphocytes in plaques, suggesting that the reactivation of CMV may contribute to the immune activation associated with the progression of atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus‐Productive Infection Is Associated With Acute Coronary Syndrome

Nikitskaya

Lebedeva

Ivanova

et al. 2016

JAHA

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“…An infectious etiology underlying atherosclerotic vascular disease has long been hypothesized (3,4). In the 1970s, arterial disease very similar to human atherosclerosis was induced by cytomegalovirus (CMV) infection in chickens.…”

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confidence: 99%

Determinants of Cardiovascular Mortality After Renal Transplantation: A Role For Cytomegalovirus?

Kalil

Hudson

Gaston³

2003

American Journal of Transplantation

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Death with a functioning graft (DWF) is now the most common cause of late renal transplant failure, with cardiovascular disease its most frequent etiology. In some populations, infection with cytomegalovirus (CMV) increases risk of coronary disease. Few data exist regarding CMV and cardiovascular mortality after renal transplantation. We reviewed charts of 158 adult patients who died more than 90 days after receiving renal allografts and a matched cohort of 143 (of 2398) surviving patients transplanted at the University of Alabama at Birmingham between 1990 and 1998. Only advancing donor and recipient age increased risk of DWF; CMV infection did not. However, of 50 patients who died of cardiovascular causes, 94% were seropositive for CMV, while only 74% of the other 108 deaths occurred in CMV-seropositive patients (p ∞ 0.05). Risk of cardiovascular death was greatest (p ∞ 0.05) in patients with diabetes, advancing age, and CMV seropositivity. In renal transplant recipients, infection with CMV increases risk of death as a result of cardiovascular causes.

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“…After the first report of an association of viral infection and atherosclerosis in 1970, 1 evidence is accumulating that infections are involved in the development and progression of atherosclerosis, with special focus on carotid and coronary lesions. 2,3 The pathogenetic mechanisms may vary and are still poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Hepatitis C virus RNA localization in human carotid plaques

Boddi

Abbate

Chellini

et al. 2010

Journal of Clinical Virology

131

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a b s t r a c tBackground: Hepatitis C virus (HCV) infection has certain characteristics that enable it to play an important role in atherosclerosis. Some studies report its association with an increased risk of carotid artery plaque. Objectives: The aim of this study was to evaluate the presence of HCV genomic sequences and replicative intermediates in plaque tissues. Study Design: A cohort of consecutive, prospectively recruited patients with HCV infection and chronic ischemic heart disease from the Cardiology, Vascular Surgery and Hepatology Units of a University Hospital in Florence, Italy, were studied. Results: Positive-strand HCV RNA was detected in seven carotid plaque tissues from anti-HCV-positive patients and was not detected in the nine carotid plaque tissues obtained from anti-HCV-negative patients. In three patients, HCV RNA was found in carotid plaque and not in serum. HCV replicative intermediates were detected in three plaque samples. Direct sequencing of HCV RNA from the plaque and serum showed HCV genotypes 2 (five cases) and 1 (two cases). Conclusions: The novel finding of HCV RNA sequences in plaque tissue strongly suggests an active local infection. This in turn makes it conceivable that the virus may exert local action in carotid atherosclerosis.

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Virus-induced atherosclerosis.

Cited by 444 publications

References 9 publications

Cytomegalovirus‐Productive Infection Is Associated With Acute Coronary Syndrome

Cytomegalovirus‐Productive Infection Is Associated With Acute Coronary Syndrome

Determinants of Cardiovascular Mortality After Renal Transplantation: A Role For Cytomegalovirus?

Hepatitis C virus RNA localization in human carotid plaques

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