The future of HIV therapeutics is brightening, according to Gladstone Institutes Director

Recent discoveries about the way that HIV infects cells are propelling the development of a broad spectrum of promising new antiviral drugs, according to an invited commentary on the topic in the current issue of Nature Immunology (August 27, 2004).

The assessment is made by Gladstone Institute of Virology and Immunology (GIVI) Director Warner Greene, MD, PhD, who also serves as professor of medicine, microbiology and immunology at the University of California, San Francisco.

In the piece, Greene points out that basic research on HIV, a relatively simple pathogen with only nine genes encoding 15 proteins, are leading to compelling new therapies that deny the initial entry of HIV into its cellular host. In addition, fast-moving research of naturally occurring factors with potent antiviral properties is opening the way for future development of an entirely new class of anti-HIV drugs.

New agents that block the first step in HIV's life cycle, the entry of the HIV virion (a single virus particle) into host CD4 T-cells, are quickly moving down the drug development pipeline. Chief among these therapeutics are drugs known as chemokine receptor antagonists that interfere with HIV's ability to bind to CCR5, one of two key surface receptors needed for the virus to penetrate the cell. Although these HIV co-receptors were identified only seven years ago, basic studies performed by both GIVI investigators and scientists around the world have helped accelerate clinical development of CCR5 antagonists as a new class of anti-HIV drugs. Several major pharmaceutical companies are now racing to the finishing line.

These advances address but one of the three steps required for successful entry of the HIV virus. The other two steps involve the attachment of HIV virions to surface CD4 receptors and the final fusion of virions to target cells. These steps are also being targeted with new antiviral drugs. Combinations of inhibitors acting at each o

Contact: John Watson
University of California - San Francisco

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