Important note: Information in this article was accurate in July 2002. The state of the art may have changed since the publication date.AIDSWEEKLY Plus; July 15, 2002
Michael Greer, Senior Medical Writer
"Treatment of patients with human immunodeficiency virus (HIV) protease inhibitors such as ritonavir can result in increases in CD4+ T-cell counts that are independent of a reduction in HIV-1 viral load," according to Shibani Pati and colleagues working at the University of Maryland and Morgan State University in Baltimore.
Ritonavir has significant anticancer effects unrelated to its HIV-inhibiting abilities, the researchers found.
Previously, Pati and coauthors discovered that ritonavir can modulate HIV virulence even without blocking the effects of viral protease. By reducing immune cell activation and apoptosis susceptibility, ritonavir creates a less fertile environment for HIV proliferation, they said.
Similarly, ritonavir treatment alters cytokine production by endothelial cells in ways that reduce the risk of Kaposi sarcoma development. The antiretroviral agent significantly lowered production of cellular factors that promote tumor angiogenesis, downregulated leukocyte adhesion molecules, and prevented transcriptional activation of the KS-promoting protein nuclear factor-(kappa) B, study data showed.
The putative anticancer effects of ritonavir were confirmed in a murine model of Kaposi sarcoma, in which the agent significantly reduced tumor development (Antitumorigenic effects of HIV protease inhibitor ritonavir: inhibition of Kaposi sarcoma, Blood 2002 May 15;99(10):3771-9.
"Taken together, these data suggest that ritonavir has antineoplastic effects that are independent from its ability to inhibit the HIV protease," Pati and colleagues concluded.
The corresponding author for this report is Frank F. Weichold, Morgan State University, Dept. of Biology, 1700 E. Coldspring Lane, Spencer Hall, Room G12, Baltimore, MD 21251, USA.
Key points reported in this study include:
This article was prepared by AIDS Weekly editors from staff and other reports.
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