6th Conference on Retroviruses and Opportunistic Infections (CROI)
HIV-Related Neoplasia: Advances and Controversies
During the AIDS epidemic one of the most common images of the face of AIDS was a drawn face with the purple-bluish cancerous lesions that were Kaposi's Sarcoma (KS). As the immune system fails, virus-caused cancers can overpower the immune system, causing severe problems, and even death.
Recently, we have seen a great deal of research done around KS, and the virus that is thought to cause KS, human herpesvirus-8 (HHV-8). HHV-8 is one of many types of herpes virus. The family of herpes virus is a group of similarly structured viruses that include cytomegalovirus (CMV), herpes simplex 1 and herpes simplex 2 (cold sores and genital herpes), and HHV-8, which has only been identified in the last few years. KS can occur internally or externally on the skin, ranging from a few small spots to extensive coverage.
The Herpes KS Connection
The presentation at the 6th Conference on Retroviruses and Opportunistic Infections (CROI) began with a discussion of two things that we don't know: How is the herpes virus HHV-8 spread and does HHV-8 cause KS?
Although researchers don't know exactly how the HHV-8 virus is transmitted, they have conducted studies and found evidence that it is transmitted sexually. One study shows that men who have sex with men are at greater risk of catching HHV-8 than others. This study demonstrated that there was a clear correlation between the number of sex partners one has and the likelihood of contracting HHV-8. Specifically, the receptive anal partners were at the highest risk for contracting HHV-8 in this study. Exposure to feces is also a possible risk factor, putting rimming and oral sex on the list of potentially risky behaviors for contracting this type of herpes. This study indicated that transmission is linked to sexual activities.
Another study examined 14 people who received blood that was infected with both the HIV virus and the HHV-8 virus (this occurred before testing was done on blood). The results were surprising. Of the 14 people who received the contaminated blood, 10 became infected with HIV but none tested positive for HHV-8.
As to whether HHV-8 causes KS, even less is known. It is a fact that one cannot get KS without having HHV-8. Thus, HHV-8 is also called KS-associated herpes virus, or KSHV. And KSHV is a tumor-causing agent that can be very aggressive. The aggressiveness of the KSHV, however, is determined by when someone contracts it. Acquiring KSHV after becoming HIV-infected seems to be the worse case scenario. In a recent study, those who got KSHV after becoming HIV+ progressed to tumors faster (within 5 years) and had much more aggressive virus than those who contracted HIV after infection after contracting HHV-8.
Advances in the Therapy of KS
Since the development of highly active antiretroviral therapy (HAART) there has been a significant decrease in the number of HIV+ people developing KS, and major progress in treatment of it. In 1994, there were only three basic options to treat KS: Interferon, radiation therapy, and chemotherapy.
Recently, new options such as liposomal anthracyclines and paclitaxel have been found to be very effective, especially in patients with advanced disease. Liposomal anthracyclines such as doxil and daunoxome are now considered to be front line agents. There is currently a trial under way looking at the effectiveness of doxil compared to paclitaxel.
But the conclusion of several researchers is that improvement of the immune system helps to prevent and control KS. The best therapy of all is keeping a strong and healthy immune system.
Back to STEP's Retroviruses Conference Coverage Index.
This article was provided by Seattle Treatment Education Project.