Exploring the potential link between human papillomavirus infection and coronary artery disease: a review of shared pathways and mechanisms.

The increasing prevalence of early onset coronary artery disease (CAD) in individuals under 50 presents a significant public health challenge, with substantial impacts on quality of life and escalating healthcare costs. Human papillomavirus (HPV), a pervasive sexually transmitted infection, has emerged as a potential contributor to atherosclerotic lesion development. This article explores the complex inflammatory pathways HPV infection activates that could contribute to atherogenesis. HPV may contribute to CAD by influencing components of metabolic syndrome. Investigating these interactions could provide new insights into disease mechanisms. The virus's capacity to cause cellular immortalization, leading to uncontrolled growth and proliferation, may also play a role in the advancement of atherosclerotic lesions in CAD patients. HPV may represent a novel risk factor for CAD, warranting further research into preventive strategies, including vaccination. This understanding opens new opportunities for effective research and intervention to address this significant public health issue. The significant association between HPV and CAD emphasizes the need for further investigation to develop preventive measures and treatment strategies, especially important for reducing the increasing incidence of CAD in younger populations.