Table Info

Table 1.

Main common and specific virus mechanisms and complications related to the increased risk of atherosclerosis

Infectious agent	Main mechanisms and pathways involved	Main CV complications
HIV	- Presence in the atherosclerotic lesion - Systemic inflammation/oxidative stress - Immunity (CD4⁺ cell depletion) - Opportunistic infections	- AMI - High prevalence of traditional CVD risk factors - Carotid atherosclerosis - Carotid stiffness - HF - Myocardial fibrosis - T2D - cART-related adverse cardiometabolic effects
HSV-1 and -2	- Presence in the atherosclerotic lesion - Systemic inflammation/oxidative stress - Endothelial dysfunction - Apoptosis - Procoagulant effects	- CV mortality - CAD - AMI - Stroke - Carotid atherosclerosis
CMV	- Presence in the atherosclerotic lesion - Systemic inflammation/oxidative stress - Host immune response - Endothelial dysfunction - Lipid dysregulation and lipid deposition, vascular SMC proliferation and migration - Procoagulant effects and increased prothrombotic risk	- Carotid atherosclerosis - CAD - AMI - Stroke - T2D
HCV	- Presence in the endothelial cells and atherosclerotic lesion - Systemic and local arterial inflammation/oxidative stress - Host immune response - Liver iron deposition - Metabolic disarrangement - Cryoglobulinemia	- CV mortality - Carotid atherosclerosis - CAD - Dysrhythmias - HF - AMI - Cerebrovascular disease - Myocarditis and Cardiomyopathies - T2D
Influenza	- Presence in the endothelial cells and atherosclerotic lesions - Systemic and local arterial inflammation/oxidative stress - Hypercoagulability - Fever, tachycardia, hypoxia-induced injury	- CV mortality - AMI - T2D
SARS-CoV-2	- Direct viral entry through ACE2 receptor (e.g., cardiomyocytes, fibroblasts, endothelial cells) - Systemic inflammation/cytokine storm - Hypercoagulability, thrombosis - Local inflammation (myocardial inflammation-myocarditis, cardiac fibrosis, myocyte apoptosis) - Plaque destabilization - Stress, anxiety, psycho-emotional status - Hypoxia-induced injury (myocardial oxygen demand/supply mismatch) - Endothelial dysfunction - Catecholamine stress response	- HF - Ventricular hypertrophy - Ventricular dilation - AMI - Fibrosis - Myocarditis - T2D

Infectious agent

Main mechanisms and pathways involved

Main CV complications

HIV

- Presence in the atherosclerotic lesion

- Systemic inflammation/oxidative stress

- Immunity (CD4⁺ cell depletion)

- Opportunistic infections

- AMI

- High prevalence of traditional CVD risk factors

- Carotid atherosclerosis

- Carotid stiffness

- HF

- Myocardial fibrosis

- T2D

- cART-related adverse cardiometabolic effects

HSV-1 and -2

- Presence in the atherosclerotic lesion

- Systemic inflammation/oxidative stress

- Endothelial dysfunction

- Apoptosis

- Procoagulant effects

- CV mortality

- CAD

- AMI

- Stroke

- Carotid atherosclerosis

CMV

- Presence in the atherosclerotic lesion

- Systemic inflammation/oxidative stress

- Host immune response

- Endothelial dysfunction

- Lipid dysregulation and lipid deposition, vascular SMC proliferation and migration

- Procoagulant effects and increased prothrombotic risk

- Carotid atherosclerosis

- CAD

- AMI

- Stroke

- T2D

HCV

- Presence in the endothelial cells and atherosclerotic lesion

- Systemic and local arterial inflammation/oxidative stress

- Host immune response

- Liver iron deposition

- Metabolic disarrangement

- Cryoglobulinemia

- CV mortality

- Carotid atherosclerosis

- CAD

- Dysrhythmias

- HF

- AMI

- Cerebrovascular disease

- Myocarditis and Cardiomyopathies

- T2D

Influenza

- Presence in the endothelial cells and atherosclerotic lesions

- Systemic and local arterial inflammation/oxidative stress

- Hypercoagulability

- Fever, tachycardia, hypoxia-induced injury

- CV mortality

- AMI

- T2D

SARS-CoV-2

- Direct viral entry through ACE2 receptor (e.g., cardiomyocytes, fibroblasts, endothelial cells)

- Systemic inflammation/cytokine storm

- Hypercoagulability, thrombosis

- Local inflammation (myocardial inflammation-myocarditis, cardiac fibrosis, myocyte apoptosis)

- Plaque destabilization

- Stress, anxiety, psycho-emotional status

- Hypoxia-induced injury (myocardial oxygen demand/supply mismatch)

- Endothelial dysfunction

- Catecholamine stress response

- HF

- Ventricular hypertrophy

- Ventricular dilation

- AMI

- Fibrosis

- Myocarditis

- T2D

CAD: coronary artery disease; AMI: acute myocardial infarction; ACE: angiotensin-converting enzyme; cART: combined antiretroviral therapy; HF: heart failure

Declarations

Acknowledgments

The author deserves special thanks to Dr. Simona Fenizia for her valuable contribution to English-style editing.

Author contributions

CV: Conceptualization, writing—original draft, writing—review & editing.

Conflicts of interest

The author declares that he has no conflicts of interest.

Ethical approval

Not applicable.

Consent to participate

Not applicable.

Consent to publication

Not applicable.

Availability of data and materials

Not applicable.

Funding

Not applicable.

Copyright

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