MEDICINE / KAPOSI’S SARCOMA : Researchers Link Herpes Strain to Skin Tumor : Once-rare condition that is now a hallmark of AIDS may be caused by previously unrecognized form of the virus, studies show. Discovery raises hope of vaccine.
Kaposi’s sarcoma, the once-rare skin tumor that has become a hallmark of AIDS, may be caused by a previously unrecognized strain of herpes virus, according to California and New York researchers.
The cause of the tumor, which strikes at least one in every four AIDS patients, has been a mystery since its increased prevalence in such patients was first noted in the early 1980s. It has been linked tenuously to a variety of viruses, as well as to the nitrite inhalants called “poppers,” but proof of such links has remained elusive.
A research team from Columbia University in New York City and DNAX Research Institute in Palo Alto reports today in the journal Science that it has isolated viral DNA that is related to herpes viruses from Kaposi’s tumor tissue. The researchers found no such DNA in non-cancerous tissue from the same patients or in tissue from healthy individuals.
The researchers are now working to identify the virus itself in hopes of producing a vaccine or some form of drug therapy. “If we can prove that this putative virus actually causes the cancer, a diagnostic test could be developed that might help clinicians determine sooner who may be at risk,” Dr. Yuan Chang of Columbia said Thursday at a news conference.
“I think it’s a tremendously interesting result,” said Dr. Harold Jaffe, head of the HIV/AIDS division of the Centers for Disease Control and Prevention in Atlanta. “At this point, we can’t definitely say it’s the (causative) agent, but I think it’s a very good candidate.”
The classical Kaposi’s sarcoma is a slow-growing skin tumor that strikes primarily elderly men of Mediterranean descent. It is characterized by purplish sores on the face and in the mouth. In AIDS patients, the disease progresses more rapidly, spreading to other organs.
Although it occasionally strikes women and heterosexual AIDS patients, Kaposi’s is primarily a disease of gay AIDS patients. As many as 50% of gay AIDS patients develop it. The two disorders are so closely associated that the presence of Kaposi’s in a young person is considered a presumptive diagnosis of AIDS.
Chang and her colleagues used a powerful new technique called representation difference analysis to identify the viral DNA. The technique allows researchers to compare two different tissue samples and isolate DNA that is present in only one.
They found the viral DNA in tissue from 25 of 27 Kaposi’s tumors and in six of 39 biopsied tissue samples from various organs of people who had AIDS but no Kaposi’s. In contrast, they found no evidence of the virus in biopsied tissues from 85 people with neither AIDS nor Kaposi’s.
Chang said Thursday that researchers in five other labs had replicated her findings. “This work has been confirmed,” she said. But the presence of the DNA in the tissues does not conclusively prove that the virus causes the tumors, she cautioned.
The virus might, for example, simply find the already-established tumor a fertile ground for growth. Proof that the virus causes the tumors will require much more work, she added.
The DNA isolated from the tumors appears to be fragments of three genes from a herpes virus. Seven types of herpes viruses have previously been isolated from humans. They cause diseases ranging from cold sores and chickenpox to genital herpes and cancer.
In a separate development that may improve the likelihood of developing an AIDS vaccine, Dr. Jay H. Levy and his colleagues at UC San Francisco report in the international medical journal The Lancet that a class of white blood cells called CD8 T-cells attack the AIDS virus during the early stages of an HIV infection.
After two to six weeks, the initial illness recedes, levels of virus in the blood fall, and neutralizing antibodies to HIV are produced. If this response of CD8 T-cells could be enhanced and prolonged, Levy said, the progression of an HIV infection to AIDS could potentially be delayed or perhaps even blocked.
Levy and his colleagues found seven HIV-infected individuals who had high levels of CD8 activity in their blood at the time they first showed HIV infection. In four of them, the activity was observed as much as one year before they became HIV-positive.
In three patients, the researchers observed a decrease in the level of HIV in the blood as CD8 activity increased, suggesting, they wrote, CD8 cells are “responsible for the control of HIV replication.”
