Impact of Infectious Burden on Progression of Carotid Atherosclerosis

Espinola‐Klein, Christine; Rupprecht, Hans‐Jürgen; Blankenberg, Stefan; Bickel, Christoph; Kopp, Helmut; Victor, Anja; Häfner, Gerd; Prellwitz, W.; Schlumberger, Wolfgang; Meyer, Jürgen

doi:10.1161/01.str.0000034789.82859.a4

Cited by 156 publications

(125 citation statements)

References 41 publications

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“…(Panel B) HCV RNA detection in serum and plaque tissue by nested RT-PCR. Lanes 1 and 11: 100 bp DNA molecular weight marker; lanes 2-10: PCR results from serum and plaque samples from two representative patients (from Table 1): patient #7 (lanes [2][3][4][5] showing HCV RNA sequences in both serum and plaque; patient #3 (lanes 7-10) in plaque tissue only. Lanes 12 and 13 (positive controls): serum sample from an HCV-positive patient and synthetic HCV RNA, respectively.…”

Section: Resultsmentioning

confidence: 99%

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Hepatitis C virus RNA localization in human carotid plaques

Boddi

Abbate

Chellini

et al. 2010

Journal of Clinical Virology

127

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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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Section: Resultsmentioning

confidence: 99%

“…2,3 The pathogenetic mechanisms may vary and are still poorly understood. Localization of the infective agent inside the plaque has been shown for most pathogens for whom a deeper evidence of such an association exists, suggesting the importance of local pathogenetic mechanism/s.…”

Section: Introductionmentioning

confidence: 99%

Hepatitis C virus RNA localization in human carotid plaques

Boddi

Abbate

Chellini

et al. 2010

Journal of Clinical Virology

127

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“…24 All these pathogens are known to directly affect vascular smooth muscle cells and/or vascular endothelial cells and to possibly cause the progression of atherosclerosis. [20][21][22][23][24][25][26][27][28][29] On the contrary, there is no evidence to date that hMPV has a direct effect on vascular smooth muscle cells or endothelial cells. hMPV is reported to affect airway epithelial cells and stimulate massive production of interleukin-8, 30,31 and regulate upon activation normal T-cell expressed and secreted.…”

Section: Discussionmentioning

confidence: 99%

Association between human metapneumovirus seroprevalence and hypertension in elderly subjects in a long-term care facility

et al. 2011

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Recently, relations between hypertension and infections caused by several pathogens have been reported. However, few studies have examined the relationship between human metapneumovirus (hMPV) and hypertension in elderly inpatients. To assess the association between anti-hMPV-immunoglobulin G (IgG) titer and the prevalence of hypertension, we conducted a case-control study in a Japanese long-term care facility (LTCF). The participants included 84 hypertensive patients aged X65 years, and 84 age-and sex-matched normotensive controls (38 males and 46 females in each group; cases, 79.9 ± 8.4 (s.d.) years; controls, 80.1 ± 8.3 years). Data on underling chronic clinical conditions were collected. Titers were measured using an immunofluorescence assay kit. The significance of risk factor differences was analyzed using univariate and multivariate comparisons of cases and controls. All serum samples were positive for hMPV, and IgG titers ranged from 40-fold to more than 5120-fold. There were no significant sex-or age-related differences in log 2 (anti-hMPV-IgG titer/10) among the subjects. Compared with normotensive subjects, hypertensive patients presented significantly higher log 2 (anti-hMPV-IgG titer/10) values (Po0.001). After adjustment with multiple logistic analysis, the odds ratio for log 2 (anti-hMPV-IgG titer/10) was 1.42 (95% confidence interval 1.16-1.75, P¼0.001) relative to normotensive subjects. In all subjects, stepwise multiple regression analysis revealed that both hypertension and a poor nutritional state independently contributed to increased log 2 (anti-hMPV-IgG titer/10). These observations suggest that an increased anti-hMPV-IgG titer was closely related to hypertension in elderly subjects in a Japanese LTCF.

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“…tarafından yapılan ve inme gelişiminin EBV IgG ile ilişkisini araştıran ça-lışmalardan biri olan araştırmada, karotisteki aterosklerozun ilerlemesinin, EBV IgG antikor yüksekliği ile ilişkili olduğu bildirilmişken, çalış-mamızda EBV IgG seropozitifliği, hasta ve kontrol grubunda benzer oranlarda bulunmuştur. 13 Birden fazla enfeksiyonun (enfeksiyon yükü) inme gelişimi üzerindeki etkisi, Espinola-Klein ve ark. tarafından araştırılmış ve çalışmalarında karotid aterosklerozun artmış enfeksiyon sayısından etkilendiğini saptamışlardır.…”

Section: Bulgularunclassified