THE VIRGINIAN-PILOT
Copyright (c) 1995, Landmark Communications, Inc.
DATE: Saturday, November 4, 1995 TAG: 9511040280
SECTION: FRONT PAGE: A1 EDITION: FINAL
SOURCE: BY MARIE JOYCE, STAFF WRITER
LENGTH: Medium: 93 lines
After years of losing the battle against AIDS, doctors are finally getting some weapons that may help them fight the virus to a draw.
``I think we're on the verge of being able to convert this into a chronic illness,'' said Dr. Edward C. Oldfield III, director of Eastern Virginia Medical School's Infectious Diseases Division.
He doesn't believe science has any prospect of vanquishing AIDS, the leading cause of death for Americans between 25 and 44. But he believes some of the newest drugs - some being tested in part in Hampton Roads - will help turn AIDS into something that can be controlled.
One drug being tested here acts by weakening the human immunodeficiency virus, the virus that causes AIDS, making it less resistant to other medicine; the other slows the virus' reproduction to a crawl.
``It's not science fiction,'' he said. The work at EVMS' Center for Comprehensive Care of Immune deficiencies is supported in part by funds collected by the annual Hampton Roads AIDS Walk for Life, to be held in downtown Norfolk Sunday from 1 p.m. to 4 p.m.
About 65 patients at EVMS's Center for Comprehensive Care of Immune Deficiencies are participating in a national trial of a drug that weakens the virus. The drug, when combined with the older drug AZT, takes advantage of one of HIV's greatest survival skills, its ability to adapt at lightening speed.
The HIV virus reproduces itself rapidly, generating 100 million new viral particles every day. Within 14 days, every bit of virus in a person's body is new. As it reproduces, it mutates rapidly - five genetic mutations with each virus, 500 million genetic mutations each day in each patient.
That constant mutation makes it a moving target, able to adjust to any weapon that science has so far thrown at it. AZT, for instance, does a good job of killing the virus initially, but loses its punch after about eight months.
The new drug, 3TC, or lamivudine, acts as a sort of a decoy. After a month of treatment, the HIV is producing offspring immune to 3TC. But the genetic change that protects it from 3TC also seems to make it particularly susceptible to AZT.
One of Oldfield's patients was carrying around 1.8 million viral particles in each milliliter - about four drops - of his blood when he started the treatment with AZT and 3TC. In three weeks, the number of viral particles was fewer than 50.
And six months later, the patient continues to experience growth in the number of immune system cells that are attacked by HIV.
``He's recovering his immune system,'' said Oldfield.
It will take some time, however, to see whether 3TC and AZT actually improve a patient's long-term survival. But the drop in viral particles means it probably will, said Oldfield.
The 3TC/AZT combination attacks the virus before it infiltrates a cell's DNA. Another type of drug makes it harder for the virus to reproduce once it has invaded.
The immune system doesn't actually shut down when hit by HIV. In fact, it works furiously, every day churning out two billion CD4 cells, the immune system cells attacked by HIV.
The only problem is that the virus kills 2 billion every day. Eventually, the body can't keep up.
Picture a sink full of water, said Oldfield. The tap on the sink is wide open and pouring. But the drain is also wide open. Eventually, the sink empties out.
Protease inhibitors, he says, ``plug the drain.''
The Norfolk clinic is participating in a trial of Crixivan, one of several different protease inhibitors under development. Half a dozen patients seen by Oldfield and his EVMS colleagues are taking part after winning a national lottery sponsored by the drug's maker, Merck & Co.
HIV reproduces by invading the CD4 cells and turning them into HIV factories. The cells create long ribbons of protein containing HIV's component parts.
The enzyme protease is a kind of organizer, clipping the ribbons of protein at exactly the right place and rearranging the chunks into the right order. Then the new packages of virus head out to infect other cells.
An inhibitor like Crixivan keeps the protease from doing its job.
Doctors envision a day when people with AIDS will take a combination of drugs like Crixivan, AZT and 3TC that will hold the disease at bay.
Developments like this give Oldfield reason to hope, a hope he tries to pass on to his patients. In fact, so much is going on in the field that he and his colleagues struggle to keep up.
Aiding this research is a new process that allows scientists to detect the progress of HIV much more quickly than before, accelerating research time.
Oldfield points out that, even without these drugs, people with HIV now may live 10 years before the virus overwhelms their immune systems.
Suppose you could stretch that to 25 years or more? A person might even live a normal life span with HIV. And other drugs that fight the symptoms can make that an active life.
``What I want is life with quality,'' he said.
KEYWORDS: AIDS TREATMENT DRUG TRIAL by CNB