Introduction
Human papillomavirus (HPV) infection is one of the most prevalent sexually transmitted diseases. The CDC estimates that there are about 20 million Americans living with the virus, with 6 million new cases each year. HPV is causally linked with cervical cancer, a cancer involving the lower end of the womb that opens into the vagina. There are about 12,000 new cases of cancer each year. HPV genetic material has been discovered in about 90 percent of cervical cancers. HPV is also linked with cancers involving other parts of the male and female genital areas, which affect more than 10,000 more adults each year.
HPV is spread almost exclusively by sexual contact. There are more than 100 strains of the virus, with about 40 strains identified in human disease. Only 30 percent of cases show up with the usual clinical presentation of viral warts involving the genitals and surrounding areas. A majority of cases of HPV are "silent" infections.
HPV and Cancer
HPV is transferred on contact. After entering the cell, the virus hijacks the cellular mechanisms to produce viral components, including genetic material. In a minority of cases, the presence of new genetic material triggers an increase in cell proliferation, leading to heaped up non-invasive growths called warts. In very rare cases, the incorporation of viral genetic material into human genetic material unhinges all the regulatory signals and sets up mechanisms that produce malignant change and invasiveness. Certain genes in the body that regulate cell division are usually inactivated, controlling sites and rate of cell division. These genes are altered by HPV to assume an uncontrollable state in the cancerous cells. This ability to produce cancerous change makes HPV an oncogenic virus.
Malignant change, leading to development of cancer, is only seen in very few cases of HPV. The strains producing viral warts do not usually produce malignant change. The strains that produce persistent (usually silent) disease lead to malignant transformation and the development of cancer. The most notorious strains in cancerous growths are HPV 16 and HPV 18.
Addendum
In the face of adequate immune responses, most cells with malignant change are picked up by the immune system and neutralized. Certain factors tend to increase the chances of successful malignant transformation among the cells infected by HPV. These include the presence of immune suppressors like HIV, co-infection with other viruses like herpes simplex type 2, long-term oral contraceptive use, smoking and multiple childbirths of five and above.
Individuals in the groups mentioned in the preceding paragraph belong to the population at high risk for cancerous growths in the presence of HPV and should be closely monitored for malignant change. Every case of HPV should receive close attention and screening for early detection of cancerous change and adequate intervention.
Immunization programs against HPV offer a big advance towards prevention of HPV and this dangerous complication.
