AIDS Update '96: New Drugs, New Tests, New Optimism Mark Recent AIDS Research
Travis, John, Science News
Imagine putting together a 50,000-piece jigsaw puzzle of an abstract painting-without a picture of the completed puzzle. First come the basics, such as identifying the four corners of the puzzle. After that, the puzzle solver painstakingly tries to marry piece after piece. As a rule, the jagged edges do not fit, and frustration mounts. On rare occasions, two pieces, maybe even three or four, snap into place and optimism emerges anew. For more than a decade, immunologists, virologists, physicians, and other researchers have attempted to piece together something much more important than a jigsaw puzzle. Their obsession is the puzzle of AIDS, the deadly syndrome caused by the infectious agent known as HIV.
Investigators have recently fitted several new pieces into the AIDS puzzle. Two months ago, researchers at the Conference on Retroviruses and Opportunistic Infections in Washington, D.C., made headlines worldwide with presentations on potent drugs called protease inhibitors and on a novel way to predict HIV's impact in patients.
The protease inhibitors, in particular, stimulated a long-absent optimism among AIDS researchers. Attesting to this newfound hope is an editorial in the March Nature Medicine entitled "AIDS-a treatable disease at last." "We're clearly at the beginning of that era," agrees Douglas D. Richman of the University of California, San Diego, an organizer of the D.C. conference. At the same time, Richman and other investigators stress that treatable doesn't equal preventable or curable. An international AIDS vaccine meeting 2 weeks after the D.C. conference barely caused a stir within the research community, largely because there has been little discernible progress in developing a preventive vaccine.
Even the much-publicized protease inhibitors, three of which have gained approval from the Food and Drug Administration, are not miracle drugs. "We'd hoped to give [a patient] a drug, get rid of all the virus, and move on. We're not nearly at that point. . . .
The best we can do is turn AIDS into more of a chronic disease," says Andrew Kaplan of the AIDS Institute at the University of California, Los Angeles (UCLA) School of Medicine. In this roundup, Science News describes some of the recent advances-and setbacks-that have made the last few months the most fascinating period in AIDS research in quite some time.
Srveying the enemy
It's tough to fight a war without knowing the size of the opponent's army, but that's the situation AIDS researchers have faced until recently. To measure the severity of an HIV infection, they were forced to rely upon secondary markers such as certain immune system cells within an infected individual. These crucial CD4 cells are the target of HIV and usually decline in number as the virus slowly overwhelms a patient's immune system. However, CD4 cell counts don't necessarily provide an accurate indication of how much virus the body is battling. They're more accurately a measure of casualties rather than enemy soldiers.
That's why scientists are excited about directly measuring viral load, the quantity of HIV in a milliliter of an infected person's blood. To gauge viral load, investigators can now count the strands of viral RNA in a blood sample. HIV stores its genetic information in strands of RNA rather than DNA. The researchers hope that monitoring changes in viral load will enable them to judge more quickly and accurately the effectiveness of new AIDS drugs.
Moreover, viral load may prove much more powerful than CD4 counts at predicting the long-term survival of an HIV-infected person. In one study presented at the D.C. conference, researchers analyzed blood samples taken in 1984 or 1985 from HIV-infected homosexual or bisexual men. At the end of a decade of follow-up, only 17 of 45 men whose viral load averaged less than 5,300 RNA strands had died of AIDS. But of 45 men whose average viral load exceeded 37,000, 34 had died (see table). …