Herpes simplex virus infection in human arterial cells. Implications in arteriosclerosis.

Hajjar, David P.; Pomerantz, Kenneth B.; Falcone, Domenick J.; Weksler, Babette B.; Grant, Angela

doi:10.1172/jci113208

Cited by 101 publications

(64 citation statements)

References 15 publications

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“…Although both groups exhibited a marked increase in cholesterol esters and triacylglyceride compared with the mock-infected group with 3-week cholesterol feeding, they also showed great standard deviation in triacylglyceride levels, reflecting individual differences in responding to the given insults. The result agrees with previous studies showing that cholesterol ester accumulation in cultured smooth muscle cells was stimulated by the infection of human herpes simplex virus type 1 (Hajjar et al, 1986;Hajjar et al, 1987). It is also noteworthy that the lipid composition of aortic lesions after virus infection and 6-week cholesterol feeding exhibited a striking similarity to those reported in the type II lesions of human atherosclerosis (Geer and Malcom, 1965;Insull and Bartsch, 1966).…”

Section: Discussionsupporting

confidence: 92%

Experimental Infection with Bovine Herpesvirus-4 Enhances Atherosclerotic Process in Rabbits

Lin

Jiang

Eng

et al. 2000

Laboratory Investigation

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SUMMARY:An association of herpesvirus and atherosclerosis has been suggested by seroepidemiologic studies and detection of the virus in arterial tissues. To facilitate the studies of the pathogenic role of herpesvirus in atherosclerosis, we established a rabbit model of atherosclerosis with bovine herpesvirus type-4 (BHV-4). Forty New Zealand White rabbits were randomly divided into six groups. Groups 1, 2, and 3 were inoculated iv with BHV-4 and control Groups 4, 5, and 6 with normal saline. Groups 1 and 4 were fed a regular diet throughout the experiment; Groups 2 and 5 were fed a diet supplemented with 2% cholesterol for 3 weeks starting at 3 weeks postinoculation; and Groups 3 and 6 with a diet supplemented with 2% cholesterol for 6 weeks starting at 3 days postinoculation. Extensive atherosclerotic lesions in Groups 2, 3, and 6, and small lesions in two rabbits in Group 1 were observed, but no obvious lesions were observed in Groups 4 and 5. BHV-4 DNA was demonstrated by polymerase chain reaction and liquid hybridization in aortic sections, various tissue samples, and peripheral blood mononuclear cells of all infected rabbits. Our studies demonstrated that BHV-4 can accelerate the atherosclerotic process in rabbits, and that experimental infection of rabbits with BHV-4 can be a useful atherosclerosis model. (Lab Invest 2000, 80:3-11).

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Section: Discussionsupporting

confidence: 92%

Experimental Infection with Bovine Herpesvirus-4 Enhances Atherosclerotic Process in Rabbits

Lin

Jiang

Eng

et al. 2000

Laboratory Investigation

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“…20 Herpesvirus infection increases aortic lipid accumulation by 2-3-fold in smooth muscle cells of chickens in vitro as well as in vivo. [21][22][23] Cholesterol uptake by the smooth muscle cells infected with Herpes simplex virus is associated with increased activity of LDL receptor, and reduced hydrolysis and efflux of cholesterol esters. 24 Moreover, Feingold et al 25 showed increased hepatic lipid and cholesterol synthesis in mice injected with various cytokines such as tumor necrosis factor alpha, interleukin-1 and interferon gamma.…”

Section: Discussionmentioning

confidence: 99%

Novel short-term effects of adenovirus Ad-36 on hamster lipoproteins

2004

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OBJECTIVE: Human adenovirus Ad-36 induces adiposity and lowers total serum cholesterol in chickens, mice and marmosets and Ad-36 antibodies are associated with human obesity. We examined the early effects of Ad-36 inoculation on plasma cholesterol levels in hamsters fed a hyperlipidemic diet. DESIGN: A total of 32 male Golden Syrian hamsters were divided into two equal weight-matched groups and intranasally inoculated with Ad-36 (INF: infected) or media (CON: control). In each group, the animals were fed either a purified diet (PF, n ¼ 8) 40%en fat 7194 mg cholesterol/1000 kcal or chow (C, n ¼ 8) ad libitum. Animals were killed 5 weeks postinoculation. RESULTS: Nested PCR assay detected Ad-36 DNA in the lung, liver, visceral adipose tissue and skeletal muscle of the INF group, but not in the CON animals. Ad-36 antibodies were detected in the INF group only. For all animals, total plasma cholesterol (TC) was not significantly affected by Ad-36 treatment (203792 vs 193775 mg/dl, P ¼ NS; INF vs CON, respectively). In 5 weeks, Ad-36 infection had no effect on TC concentration in hamsters fed chow (128739 vs 130727 mg/dl, INF-C vs CON-C, respectively) or those fed PF (269770 vs 256747 mg/dl, INF-P vs CON-P, respectively). However, lipoproteins isolated by density gradient ultracentrifugation showed a greater proportion of LDL cholesterol in INF animals, as compared to CON (28.471.6% vs 16.471.2%, P ¼ 0.02), regardless of dietary treatment (INF-P vs CON-P: 27.372.1 vs 15.771.5%, P ¼ 0.07; and INF-C vs CON-C: 29.471.2 vs 17.071.1%, P ¼ 0.009). This shift appears to be from HDL cholesterol to the LDL fractions. CONCLUSION: These data suggest that in the hamster (a model resembling several aspects of human lipoprotein metabolism), Ad-36 infection may acutely affect the intravascular processing of lipoproteins resulting in a more atherogenic lipoprotein profile.

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“…The likelihood that pathogen burden is not just a surrogate marker for some other factor or factors is suggested by the extremely high risk posed (Table 3) and the many mechanistic studies that demonstrate pathogens evoke cellular changes that in themselves could account for the development of atherogenesis and for the precipitation of the acute complications of atherosclerosis. [22][23][24] One potential confounding influence not evaluated in the present study that could influence our conclusions is the impact of socioeconomic status (SES). Unfortunately, we cannot address this issue definitively because information related to SES was not obtained as part of the database.…”

Section: Zhu Et Al Multiple Infections and MI Or Deathmentioning

confidence: 99%

Prospective Study of Pathogen Burden and Risk of Myocardial Infarction or Death

Zhu

Nieto²,

Horne³

et al. 2001

Circulation

244

166

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Background-We previously demonstrated that the risk of coronary artery disease (CAD) increased in relation to the number of pathogens (the "pathogen burden") in a cross-sectional study. In the present prospective study with a different patient cohort, we evaluated the effect of pathogen burden on the risk of myocardial infarction (MI) or death among CAD patients. Methods and Results-IgG antibodies to cytomegalovirus (CMV), hepatitis A virus (HAV), herpes simplex virus type 1 (HSV1), HSV type 2 (HSV2), Chlamydia pneumoniae and Helicobacter pylori, and C-reactive protein (CRP) levels were tested in baseline blood samples from 890 patients who had significant CAD on angiography. The mean follow-up period was 3 years. The baseline prevalence of antibodies directed against CMV, HAV, HSV1, or HSV2, but not C pneumoniae and H pylori, was significantly higher among patients who subsequently developed MI or death than among control subjects. After adjustment for traditional risk factors, number of diseased vessels, and clinical presentation, relative hazards (95% confidence limits) for MI or death were 2.0 (1.4 to 3.2) for CMV, 1.6 (1.1 to 2.3) for HAV, and 1.5 (1.0 to 2.2) for HSV2. Increasing pathogen burden was significantly associated with increasing risk of MI or death in a dose-response fashion. Adjusted relative hazards of MI or death associated with pathogen burden were significant among individuals with low or high CRP levels. Conclusions-The

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Herpes simplex virus infection in human arterial cells. Implications in arteriosclerosis.

Cited by 101 publications

References 15 publications

Experimental Infection with Bovine Herpesvirus-4 Enhances Atherosclerotic Process in Rabbits

Experimental Infection with Bovine Herpesvirus-4 Enhances Atherosclerotic Process in Rabbits

Novel short-term effects of adenovirus Ad-36 on hamster lipoproteins

Prospective Study of Pathogen Burden and Risk of Myocardial Infarction or Death

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