Atherosclerosis by Virus Infection—A Short Review

Jung, Seang-Hwan; Lee, Kyung Tae

doi:10.3390/biomedicines10102634

Cited by 13 publications

(11 citation statements)

References 98 publications

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“…Cardiovascular disease (CVD) remains a leading cause of mortality, contributing significantly to the global disease burden. Despite advances in identifying traditional risk factors, such as smoking, hypertension, and dyslipidemia, residual risk of CVD persists, part of which has been postulated to be induced by viral infection 1,2 . The recent pandemic of coronavirus disease 2019 (COVID‐19) has amplified public awareness regarding the potential cardiovascular complications that can arise postviral infection 1,3 .…”

Section: Introductionmentioning

confidence: 99%

“…This results in a state of low‐grade chronic inflammation, which is known to contribute to a range of age‐related inflammatory diseases, including atherosclerosis, exacerbating the development and progression of CVD 8 . Previous studies have highlighted shared pathways of viral infection‐related inflammation and atherosclerosis, such as cellular senescence, endothelial injury, lipid accumulation, coagulation, and thrombosis 1,9 …”

Section: Introductionmentioning

confidence: 99%

“…Despite advances in identifying traditional risk factors, such as smoking, hypertension, and dyslipidemia, residual risk of CVD persists, part of which has been postulated to be induced by viral infection 1,2 . The recent pandemic of coronavirus disease 2019 (COVID‐19) has amplified public awareness regarding the potential cardiovascular complications that can arise postviral infection 1,3 . This concern extends to other viruses that exhibit potential cardiovascular impact, such as herpes simplex virus (HSV), human papillomavirus (HPV), hepatitis virus, cytomegalovirus (CMV), and human immunodeficiency virus (HIV), many of which are known for chronically infecting human and widespread prevalence 2,4 .…”

Section: Introductionmentioning

confidence: 99%

“…8 Previous studies have highlighted shared pathways of viral infection-related inflammation and atherosclerosis, such as cellular senescence, endothelial injury, lipid accumulation, coagulation, and thrombosis. 1,9 Considering the widespread prevalence of chronic viral infection and its long-standing impact to human body, it is critical to explore its relationship with adverse health outcomes from a population-based perspective. Epidemiological studies have increasingly linked certain chronic viral infections with elevated risk of CVD, such as HSV, hepatitis C virus (HCV), CMV, HPV, and HIV.…”

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confidence: 99%

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Association between chronic viral infection‐related hospitalization and risk of cardiovascular disease: A population‐based cohort study

Yang,

Lu,

Bian

et al. 2024

Journal of Medical Virology

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Chronic viral infection induces immunosenescence and systemic low‐grade inflammation, leading to worsened long‐term outcomes. We sought to explore the short‐ and long‐term effects of chronic viral infection on cardiovascular disease (CVD). Based on UK Biobank data, exposed group was identified as individuals who had chronic virus infection‐related hospitalization (IRH). Unexposed group was randomly selected, matched by 5‐year age interval, sex, and Charlson comorbidity index at a ratio up to 1:10. Restricted cubic splines were used to model time‐varying effects of IRH in nonproportional Cox models. A cut‐off value of 5 years was recorded and used in piecewise Cox proportional hazards models as we estimated short‐ and long‐term effects of IRH on CVD. A total of 2826 exposed participants and 28 212 matched unexposed participants were included. Chronic viral IRH was associated with increased risk of CVD (0–5 years: hazard ratio, 1.57 [95% confidence interval: 1.32, 1.87] and 5+ years: 1.31 [1.06, 1.61]). Elevated risk of stroke was only observed within the initial 5‐year follow‐up (0–5 years: 1.91 [1.30, 2.81]). The short‐ and long‐term associations were observed in herpes or hepatitis virus IRH with risk of CVD (all p < 0.05). Subgroup analysis revealed long‐term association between chronic viral IRH and CVD among female (5+ years: 1.68 [1.27, 2.22]) but not among male. The association between chronic viral infection and elevated CVD risk appeared to be stronger among individuals who did not take cholesterol‐lowering medication, antithrombotic medication, or certain antihypertensive medications (all p for interaction < 0.05). The risk of CVD event remained persistently higher within and over 5 years following chronic viral IRH, especially in individuals infected with herpes and hepatitis virus.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Association between chronic viral infection‐related hospitalization and risk of cardiovascular disease: A population‐based cohort study

Yang,

Lu,

Bian

et al. 2024

Journal of Medical Virology

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“…There is evidence to suggest that inflammation is a key factor in the development and progression of atherosclerosis ( Ballantyne and Nambi, 2005 ). Chronic infection with various pathogens may trigger inflammatory responses in blood vessel walls, which may be crucial in the development of atherosclerosis and the progression of coronary heart disease (CHD) ( Epstein, 2002 ; Zhu and Liu, 2020 ; Jung and Lee, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

Causality of anti-Helicobacter pylori IgG levels on myocardial infarction and potential pathogenesis: a Mendelian randomization study

Wang,

Liu,

et al. 2023

Front. Microbiol.

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BackgroundPrevious observational studies have shown that a potential relationship between anti-Helicobacter pylori (H. pylori) IgG levels and Myocardial Infarction (MI). Nevertheless, the evidence for the causal inferences remains disputable. To further clarify the relationship between anti-H. pylori IgG levels and MI and explore its pathogenesis, we conducted a Mendelian randomization (MR) analysis.MethodsIn this study, we used two-sample Mendelian Randomization (MR) to assess the causality of anti-H. pylori IgG levels on MI and potential pathogenesis, 12 single nucleotide polymorphisms (SNPs) related to anti-H. pylori IgG levels were obtained from the European Bioinformatics Institute (EBI). Summary data from a large-scale GWAS meta-analysis of MI was utilized as the outcome dataset. Summary data of mediators was obtained from the FinnGen database, the UK Biobank, the EBI database, MRC-IEU database, the International Consortium of Blood Pressure, the Consortium of Within family GWAS. Inverse variance weighted (IVW) analysis under the fixed effect model was identified as our main method. To ensure the reliability of the findings, many sensitivity analyses were performed.ResultsOur study revealed that increases of anti-H. pylori IgG levels were significantly related to an increased risk of MI (OR, 1.104; 95% CI,1.042–1.169; p = 7.084 × 10−4) and decreases in HDL cholesterol levels (β, −0.016; 95% CI, −0.026 to −0.006; p = 2.02 × 10−3). In addition, there was no heterogeneity or pleiotropy in our findings.ConclusionThis two-sample MR analysis revealed the causality of anti-H. pylori IgG levels on MI, which might be explained by lower HDL cholesterol levels. Further research is needed to clarify the results.

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The pressing need for study on the effects of Mpox on the progression of vascular inflammation: A well‐timed call

Meem,

Proma,

Bhuiyan

et al. 2024

Health Science Reports

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BackgroundThis article explored the possibility that the Mpox virus (MPXV) may initiate or stimulate the consequences of vascular inflammation. In 1970, it was discovered that Macaca cynomolgus primates infected with MPXV also infected humans in the Democratic Republic of the Congo.DiscussionThe study demonstrates that MPXV invades host cells via viral proteins and surface receptors, initiating the release of diverse inflammatory mediators such as IL‐1, IL‐6, TNF‐α, CCL2, CXCL2, CXCL8, CXCL10, and so forth probably through endothelial dysfunction by reactive oxygen species production. In general, these mediators have been found to contribute to vascular inflammation and the formation of atherosclerotic plaque at a later stage, which may contribute to the onset of vascular inflammation.ConclusionThe discussed association between vascular inflammation and Mpox has the potential to be an important finding in the field of vascular biology research.

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Atherosclerosis by Virus Infection—A Short Review

Cited by 13 publications

References 98 publications

Association between chronic viral infection‐related hospitalization and risk of cardiovascular disease: A population‐based cohort study

Association between chronic viral infection‐related hospitalization and risk of cardiovascular disease: A population‐based cohort study

Causality of anti-Helicobacter pylori IgG levels on myocardial infarction and potential pathogenesis: a Mendelian randomization study

The pressing need for study on the effects of Mpox on the progression of vascular inflammation: A well‐timed call

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