HHV-8 Found in Saliva, Suggests Spread by ‘Deep Kissing’

SEATTLE—A new study shows that human herpesvirus 8 (HHV-8), thought to be the cause of Kaposi’s sarcoma, is more likely to be found in mucosal samples than in anal/genital samples, and is found at higher levels in saliva than in samples from the genital tract. Consequently, viral spread is more likely from oral than from genital exposure.

“Among specific sexual behaviors with HIV-positive partners, only deep kissing was significantly associated with seropos-itivity for HHV-8,” said Lawrence Corey, MD, of the Program in Infectious Diseases, Fred Hutchinson Cancer Research Institute.

Mucosal spread of HHV-8 could explain some “puzzling epidemiologic aspects” of HHV-8 infection, said Dr. Corey and his colleagues at Hutchin-son, the University of Washington, Seattle, and the University of Minnesota.

For example, HHV-8 infection is common in regions of Africa and Italy; it is often acquired in early childhood with increasing rates of seropositivity with age. “This suggests that nonsexual modes of transmission may be important in these regions,” Dr. Corey said.

The study cohort included 112 homosexual men with no clinical evidence of Kaposi’s sarcoma, enrolled from 1998 to 1999. Among these, 39 were HHV-8 positive and 27 agreed to participate in the HHV-8 study. Sixteen were HIV negative, and 11 were HIV positive.

The researchers used PCR assays to detect HHV-8 DNA in 880 samples taken from these 27 men. The study showed that HHV-8 DNA was found more frequently in oral cavity samples—saliva (12%), pharyngeal swabs (11%)—than in genital tract samples (4%) and anal swabs (2%). The virus was found in 5% of semen samples (N Engl J Med 343:1369-1377, 2000).

Oral cavity secretions also had the highest number of copies of HHV-8 DNA. The geometric mean titer of virus detected in saliva samples was 4.3 log copies/mL and in pharyngeal swabs, 3.1 log copies/mL, compared to 1.6 log copies/mL for samples from all others sites.

The researchers also looked at an earlier cohort of 23 HHV-8 seropositive homosexual men who had undergone more extensive sampling and found similar results. HHV-8 DNA was found in 34% of oropharyngeal samples (382 of 1,134), compared with 0.35% of urethral samples (3 of 848) and 1% of anal samples (11 of 1,087).

To evaluate risk factors for HHV-8 infection, the researchers looked at the 92 HIV-negative men from the original cohort of 112. Of this group, 66 were HHV-8 negative, and 26 were HHV-8 positive.

On multivariate analysis, the researchers reported, three factors independently predicted positive HHV-8 status: a history of deep kissing with an HIV-positive partner, a history of having a partner with Kaposi’s sarcoma, and the use of amyl nitrite capsules (“poppers”) or inhaled nitrites in association with sex.

If HHV-8 is spread through kissing, the researchers asked, then why is it not more common in the general population in North America? They suggested that the virus may not be easily transmitted.

“Acquisition may depend on the degree of exposure to infected persons, especially those who are immunocompro-mised,” they said. There also may be unidentified cofactors that increase either viral shedding in infected persons or the risk of infection in uninfected persons.

The researchers said that more than 39% of people infected with both HIV and HHV-8 ultimately develop Kaposi’s sarcoma. Yet few homosexual men practice protected oral sex, and oral-oral contact such as deep kissing is not generally recognized as a high-risk behavior for transmission of sexually transmitted diseases.

“Until we have a better understanding of the mechanisms of transmission, it will be difficult to define the most effective approach to prevention [of Kaposi’s sarcoma],” the investigators said. “Our findings suggest that safer sex practices such as consistent use of condoms, although important in preventing other sexually transmitted infections, may not protect against HHV-8 infection.”