The Bay Area Reporter - July 23, 1996
Jeff Getty, ACT UP/Golden Gate Writers Pool

Recent news reports indicate that researchers Feng, Broder, and Berger at the NIH have found a novel protein on human cells called fusin, which helps HIV bind to immune cells. And most recently, a collaboration of scientists from Aaron Diamond AIDS Research Center and Rockefeller University discovered another major co-receptor for HIV called CC-CKR-5. But what is fascinating is that the chemokines RANTES, MIP-l? and MIP-1? seem to have a high affinity for the newly discovered CC-CKR-5 receptor site. It is thought that the chemokines either block HIV binding to cells by sticking to CC-CKR-5 sites, or that perhaps the chemokines presence changes the cells CC-CKR-5 receptor in a way that stops HIV from grabbing hold.

"I think these are good hypotheses, the simplest being that the chemokines in non-progressors block HIV from interacting with the new co-receptors," said Rachel Gerstein, a Stanford University researcher. "There may be more complex phenomenon going on behind these observations. I think it's very exciting that there are more than one co-receptors, [which] seems to explain the targeting of the virus to specific types of cells.

"Its a good example of how clinical and basic research inform each other. There has to be a reason why some people do not progress to AIDS, and so the finding that the chemokines are higher in non-progressors seems to be least part of that reason," Gerstein observed.

Where does fusin play into the puzzle? Gerstein speculates that certain strains of HIV require fusin to infect cells. "My guess is that people are going to try to find out a lot more about fusin and its ligand [an inter-cellular molecule associated with a surface receptor] in the very near future." According to the June 1996 issue of Nature, new factors, as yet undiscovered, may also help block HIV from using the fusin receptor.

In the June 1996 issue of Science, author Robin Weiss speculates that later in HIV infection, more virulent syncytium inducing (unwanted clumping of infected T-cells) infections are probably the results of HIV changing binding sites from CC-CKR-5 to fusin. Weiss suspects that HIV mutation might be influenced by the virus's need to find new co-receptors. Also other HIV strains such as HIV2, found more often in IV drug users, may be able to infect a broader range of CD4 T-cells by using several different undiscovered co-receptors.

Gary Nolan, another Stanford University HIV researcher, speculates that the virus can respond in an evolutionary way in the body to adapt to different cell types. Early on in infection it may not access cells because of chemokine receptor blocking. As the immune system depletes, the chemokines may also deplete because of general disturbances in the system. "A researcher in our lab, David Zapol, will most likely be applying our intercellular peptide libraries against the new receptor. He hopes to block HIV binding or fusion to immune cells," Nolan announced.

The discovery of fusin and CC-CKR-5 receptors may also lead to the finding that certain genetic differences between humans could effect the placement and shape of these receptors. Perhaps people who have HIV for years and never progress to AIDS have different versions of fusin and CC-CKR-5.

These new cell receptors probably explain why heretofore only humans get HIV and AIDS. Scientists now believe that these new cell receptors can be grown in other animals, such as rabbits. For the first time, researchers may be able to study AIDS in animals other than humans - opening the door to understanding about how HIV destroys immune cells.

The latest new findings, and the linkage between old and new discoveries is unprecedented in HIV research. Not since the discovery of the CD4 receptor, a decade ago, have we learned as much about HIV. There is guarded optimism among many that pharmaceutical interventions targeting these new receptors or enhancing anti-HIV chemokine production may soon be at hand. Or perhaps there may be a more natural way to stimulate the body to produce beneficial chemokines such as RANTES, using alternative therapies and or herbs.

ACTion UPdate:

Growth (hormone) is evidence of change

The FDA is in the process of approving Growth Hormone for AIDS wasting this week. Thanks to your calls and faxes, the government has found a way to increase options for people with wasting. Keep the pressure on! Call or fax Janet Woodcock or Jim Lumpkin at the FDA: phone (301) 594-5401 fax (301) 594-6197.

ACT UP/Golden Gate meets every Tuesday evening at 7:30 p.m. at 592-B Castro Street in SF. The public is welcome.
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