Human papilloma virus and atherosclerotic cardiovascular disease

Graphical Abstract Human Papilloma virus (HPV) is a non-enveloped DNA virus that infects cervical epithelial cells and is a known cause of cervical cancer in women. Less known are the findings of recent epidemiological studies that associate HPV with a higher risk of atherosclerotic cardiovascular morbidity and mortality. There are at least two possible ways in which HPV infection can contribute to this process and its complications. First, HPV could directly invade atherosclerotic plaques, thereby causing plaque progression and/or instability. Although the prevailing opinion is that HPV is an infection limited to epithelial cells, some authors have reported the detection of HPV DNA and protein in atheromatous coronary arteries as well as in endothelial cells, smooth muscle cells, plasma cells and foamy macrophages located in these plaques. The transport mechanism to infect distant sites is still being elucidated but a possibility is that extra-cellular vesicles, which contain HPV DNA released from infected cells, transport the viral elements in blood to other sites. Second, HPV infection could trigger a systemic inflammatory response (including inflammasome activation) that accentuates atherosclerosis and promotes plaque instability. Human Papilloma virus (HPV) is a non-enveloped DNA virus that infects cervical epithelial cells and is a known cause of cervical cancer in women. Less known are the findings of recent epidemiological studies that associate HPV with a higher risk of atherosclerotic cardiovascular morbidity and mortality. There are at least two possible ways in which HPV infection can contribute to this process and its complications. First, HPV could directly invade atherosclerotic plaques, thereby causing plaque progression and/or instability. Although the prevailing opinion is that HPV is an infection limited to epithelial cells, some authors have reported the detection of HPV DNA and protein in atheromatous coronary arteries as well as in endothelial cells, smooth muscle cells, plasma cells and foamy macrophages located in these plaques. The transport mechanism to infect distant sites is still being elucidated but a possibility is that extra-cellular vesicles, which contain HPV DNA released from infected cells, transport the viral elements in blood to other sites. Second, HPV infection could trigger a systemic inflammatory response (including inflammasome activation) that accentuates atherosclerosis and promotes plaque instability.