Cardiovascular Consequences of Oncogenic Viral Infections: Investigating the Dual Threat

Author(s): Juweria Shahrukh Effendi, Ali javeed, Omar Saafan, Mohamed Abdelfattah, Sarath Vayolipoyil, Nisarg Shah, Sanjay Raguseelan

The cardiovascular diseases (CVD) continue to pose a significant worldwide health concern with an increasing effect on mortality despite progress in the management of traditional risk factors. There is increasing recognition that both direct and indirect mechanisms of viral infections, including human papillomavirus (HPV) and members of the Flaviviridae family, such as hepatitis C virus (HCV), dengue virus and Zika virus, play a role in cardiovascular disease (CVD). According to recent data, a chronic HPV infection may increase the risk of atherosclerotic cardiovascular disease (ASCVD) possibly through systemic inflammation and viral oncoprotein mediated endothelial dysfunction. The chronic inflammation, metabolic abnormalities, immune complex deposition and direct endothelial damage are the mechanisms by which chronic HCV infection is associated with accelerated atherosclerosis, microvascular disease and elevated cardiovascular event rates. There are many diseases like myocarditis, arrhythmias and heart failure that are the main acute cardiovascular consequences caused by Flaviviridae-related arboviral infections including dengue and Zika. These infections are caused by disruption of the endothelium barrier, cytokine storms and autonomic instability. The antiviral therapies especially direct-acting antivirals (DAAs) for HCV showed promise in lowering the risk of CVD by reducing inflammation produced by viremia. This synthesis emphasizes the possibility for tailored antiviral therapies to function as cardio protective measures and stresses the significance of incorporating viral infection status into cardiovascular risk assessment.