AIDSWEEKLY Plus; August 19, 2002
Staff Medical Writer

The research, published online July 14, 2002, by Nature, shows how CEM15 would stop HIV infection, but is normally overcome by a small HIV protein called Vif (virion infectivity factor), that suppresses its activity. Although scientists know that Vif plays an essential part in ensuring HIV replication, its precise functions have remained unclear.

Professor Michael Malim at King's, together with Dr. Ann Sheehy and other colleagues at the University of Pennsylvania School of Medicine, studied cells infected with a form of HIV that lacked Vif. They found that the CEM15 gene interfered with the HIV life cycle, rendering any new virus particles noninfectious.

"These are very significant findings and could open the door to new treatments for HIV/AIDS in the future," said Malim, head of infectious diseases at King's College London. "Previous studies have shown that Vif is crucial in infection and neutralizes some sort of defense system in healthy cells. Our research has identified CEM15 as a key component of the system in question. If we can find a way to block the action of Vif, it would allow CEM15 to work properly and prevent HIV from spreading.

"When a virus such as HIV infects a cell, it basically comes with its own blueprints in the form of RNA and a few proteins that act as tools. Using just this, it hijacks the cell's entire biochemical machinery, turning it into a factory that churns out new viruses, or virions. These virions then go on to infect and kill other cells and so the cycle continues.

"There is still a lot to learn about Vif. Ongoing work includes identifying substances that bind to and inhibit Vif in the cell, elucidating its precise mechanisms of action and structural studies of the protein. All this research will hopefully lead to a way of stopping Vif from working and thus enabling the body's natural defense mechanism to come into play."

Combination therapies using multiple antiviral drugs that target two important elements in the HIV cycle, reverse transcriptase and protease, remain the best way to treat HIV at the moment. However, this does not lead to the total disappearance of the virus and the virus develops resistance to these drugs in about half of all treated patients. This is why research for other antiviral drugs which can target other parts of the HIV replication cycle is so important (Sheehy AM, Gaddis NC, Choi JD, et al. Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein. Nature, July 14, 2002;www.nature.com).

"Therapies based on another of the key viral proteins (Env), that allows HIV to enter and infect cells, are currently being tried with some success in clinical trials, so there is the potential for further research on Vif to lead to a new way to tackle HIV," Malim concluded. "It's very ambitious, but we may see Vif developed as a new target for therapy in the next 10 years."

This article was prepared by AIDS Weekly editors from staff and other reports.

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