The virus blamed for nearly all cases of cervical cancer and suspected in a host of other human cancers appears to be linked to one of the most common skin cancers, researchers said today.

Certain strains of a widespread virus called human papillomavirus were associated with increased risks of developing squamous cell carcinoma, according to findings published online in the British Medical Journal.

Different strains of the virus, which is passed through physical contact, are thought to be behind genital warts as well cancers of the mouth, throat, anus, vulva and penis.

Previously, DOTmed reported on research suggesting the virus was also responsible for an upswing in the occurrence of squamous cell carcinoma in the mouth and throat.

Squamous cell carcinoma is the second most common skin cancer in the United States, after basal cell carcinoma, according to the American Academy of Dermatology, accounting for one-fifth of all new skin cancer cases.

HPV has been linked to skin cancer before, though largely only for organ transplant recipients and for those suffering from a rare genetic disorder that makes people susceptible to HPV and causes warty lesions to break out all over the body, called epidermodysplasia verruciformis, the authors said.

In the current study, researchers found that people infected with several types of HPV, called beta HPV, were more than one and one-half times more likely to have squamous cell carcinoma than those uninfected.

The more strains of the bug people were infected with, the greater the risk for the disease, researchers discovered. Patients taking immunosuppressive drugs and infected with HPV were at most risk for the cancer.

"We detected an excess risk of squamous cell carcinoma associated with all beta human papillomaviruses examined and a clear increasing trend in risk with increasing number of beta types to which a person tested positive," wrote the authors, led by Margaret R. Karagas, a professor of biostatistics and epidemiology at Dartmouth Medical School in Hanover, N.H.

For the study, the researchers studied 2,366 people in New Hampshire between July 1993 and June 1995, and then between July 1997 and March 2000, interviewing most of the participants.

Around 663 of the participants had squamous cell carcinoma, 898 had basal cell carcinoma and 805 were healthy age- and sex-matched controls.

They also took blood samples of patients to check for antibodies to 16 strains of beta HPV.

Although no relationship was found between HPV and basal cell carcinoma, infection appeared to up the risk for squamous cell carcinoma.

And the more strains of beta HPV they were infected with, the less merry: Patients with skin cancer were about 1.4 times more likely to test positive for antibodies to two or three strains of HPV, but they were 1.7 times more likely to test positive to more than eight types of the virus, the authors said.

Other trends emerged, too. Long-term users of glucocorticoids, which weaken the immune system, who had HPV antibodies were more than three times more likely to have skin cancer than nonusers, the authors said, although this finding had little statistical power because of the small numbers of patients in the study who were on the medications.

Patients with cancer and HPV were also nearly twice as likely to have sensitive skin and have endured a severe, blistering sunburn, although a weaker relationship was found with the number of lifetime sunburns.

The sunburn connection is expected, as squamous cell carcinoma has a known relationship with ultraviolet light exposure. The researchers also suggest a protein in the virus might prevent the body from killing off cells damaged by UV rays.

Still, because of the study design, the researchers couldn't tell what the patients got first: HPV or the cancer. To control for that, the researchers tested blood samples from a separate group of patients who were part of a cancer trial before and after diagnosis of skin cancer. They didn't find that HPV infection rates jumped up after cancer diagnosis, as would be found if the cancer somehow made the infections more likely, and not vice versa.

"On the whole, it thus seems unlikely that our observations were due simply to higher antibody titres resulting from disease onset," the authors said.