CardioExchange Archive

Human papillomavirus (HPV) may play a role in the development of cardiovascular disease (CVD) in women, according to a new study published in the Journal of the American College of Cardiology.

Hus-Ko Kuo and Ken Fujise speculated that HPV may be a risk factor for CVD because it inactivates the tumor-suppressor protein p53, which plays a regulatory role in atherosclerosis. They analyzed data from 2450 women aged 20 to 59, 60 of whom reported having coronary artery disease.  About 47% of all the women were HPV-positive, as assessed by a DNA analysis of self-collected vaginal swab specimens.

Among the women with CVD, 39 were HPV-positive while 21 were negative. After adjusting for age and race, the investigators found that HPV elevated the risk for CVD by two-and-a-half times. This increase remained significant when other risk factors were also included in the analysis. Women with cancer-associated HPV types had an even higher risk elevation.

The authors write that to the best of their knowledge there has been “no previous report on the association between HPV and CVD.”

The article is accompanied by an editorial written by Joseph Muhlestein, who more than a decade ago first proposed that a different infectious agent, Chlamydia pneumoniae, might play a causative role in CVD. He writes that

…the present article adds another important infectious candidate to the list of agents associated with the development, progression, or destabilization of atherosclerotic cardiovascular disease. This finding re-emphasizes the potential roles that a variety of chronic infectious agents may play in the pathogenesis of atherosclerosis. Despite setbacks experienced in a number of clinical trials designed to treat patients based on the “infectious hypothesis,” it still lives on, and slowly, progress is being made.

“In the end,” he concludes, “the infectious hypothesis of atherosclerosis may still pan out.”