No association between a herpesvirus infection and pulmonary hypertension

Jan 30 2005

Contrary to the results of a recent U.S. study, investigators in Japan found no association between a herpesvirus infection and a potentially life-threatening form of high blood pressure, as reported in the March 1 issue of The Journal of Infectious Diseases, now available online.

The researchers reported that they were not able to detect human herpesvirus 8 (HHV-8), also known as the Kaposi’s sarcoma virus, in the lungs of 22 patients with primary or other forms of pulmonary hypertension. These observations, by Harutaka Katano and colleagues from Toho University School of Medicine and the National Institute of Infectious Diseases in Tokyo, Japan, contrast with those in a much-publicized 2003 article published in The New England Journal of Medicine that reported the presence of the virus in similar samples of lung tissue from a similar number of patients.

Both primary pulmonary hypertension and infection with HHV-8 are uncommon, Katano and co-authors explained. Human herpesvirus 8 infection is associated with Kaposi’s sarcoma, a type of cancer most commonly seen in some parts of Africa and southern Europe and in people infected with HIV. Primary pulmonary hypertension is characterized in part by vascular lesions in the lung, and may lead to heart failure. Some cases are associated with genetic susceptibility, the investigators noted, but the pathogenesis of most cases is not known.

Dr. Katano and colleagues conducted their research using a design similar to that in the earlier study: a retrospective analysis of pathology specimens from a small number of subjects. They looked for evidence of HHV-8 in samples of lung tissue from 10 patients diagnosed with primary pulmonary hypertension at a Tokyo hospital from 1981 to 2003. They also examined samples of lung tissue from 12 patients with other forms of pulmonary hypertension. All 22 were Japanese. For a control group, the scientists studied Kaposi’s sarcoma tissue samples obtained from unrelated patients.

Like the authors of the earlier study, Katano and colleagues performed two types of tests in the tissue samples, one to detect an antigen associated with HHV-8, the other to detect HHV-8 DNA. Both tests failed to detect either the antigen or the DNA in any of the 22 samples from the two groups with some form of pulmonary hypertension, whereas the antigen was detected in the control group of Kaposi’s sarcoma tissue samples.

These data suggest that human herpesvirus 8 infection is not associated with Japanese cases of primary pulmonary hypertension, the investigators concluded. In contrast, the 2003 study identified evidence of HHV-8 in ten of 16 samples from U.S. patients with primary pulmonary hypertension.

The researchers noted that while their results call the earlier study results into question, there are other possible explanations for the divergent data. For example, the pathogenesis of primary pulmonary hypertension in Japan may be different from that in the United States. The sensitivity and methods of the tests used in each study may also have differed.

“We hope that our results provide scientists with another perspective on the potential causes of primary pulmonary hypertension,” Dr. Katano said. “Further studies are required to clarify the possible association of human herpesvirus 8 with this disease.”

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