Prescription Hope

Richard Eastman, a longtime Hollywood promoter known for his campaign to save the Hollywood Sign, put off getting tested for HIV. He was healthy, gay, engaged in safer sex, and just didn't want to think about morbid things. Then, two years ago, his weight began to drop and he got a bad cold.Like many men and women, he didn't learn he had AIDS until he was struck with a bout of Pneumocystis carinii pneumonia, an opportunistic infection associated with the virus. As he gasped to breathe at L.A. County USC Medical Center, he feared his days were few. He tried d4T (an AZT-like antiviral) and went home, but his health improved only briefly. After a few months, his disease-fighting white blood cells known as T-helper cells plummeted from 118 cells per mm3 of blood to a handful.That's when Eastman met Dr. Charles Farthing, the medical director of AIDS Healthcare Foundation, and learned about human trials with promising new experimental drugs that were "supposed to fight HIV as never before." Eastman struggled with the most important questions of his life: Did he want to gamble on the latest, greatest AIDS drugs? Hadn't the AIDS community been duped by science before?Despite awful -- and deserved -- press on drugs that have been reputed to battle HIV, Eastman figured he had nothing to lose. He became one of only 40 local participants in an initial 1995 worldwide study of protease inhibitors involving 1,200 patients. "It was so early in the process," he recalls, "that the medicine wasn't even in pill form, and we had to drink this horrible liquid three times a day."But the "rotten sock" taste paid off, and Eastman, like many, experienced a dramatic boost in his health. His T-cells jumped from 22 to 108 -- "almost a miracle, considering that with AZT they just jumped 10 or 20 points at most." By the second month on protease inhibitors, he felt good, required fewer naps and began to regain weight. Then, his T-cells jumped from 108 to 265.Psychologically, such an increase means the world to a person living with AIDS. The Centers for Disease Control defines clinical AIDS as occurring when the T-cell count dips below 200. "I feel good about surviving, getting back to work, having a normal life," Eastman says today. "Who would have thought about having hope again?"Hope is not a word people with AIDS use when it comes to AIDS medicine. "Crushing disappointment" is more like it. From Bitter Melon to AZT to Suramin to Compound Q, Persons With AIDS (PWAs) have been betrayed by drugs designed to help them fight HIV that instead make them sicker -- or kill them. Aside from Band-Aid drugs designed to help collapsing immune systems stave off fatal infections, PWAs haven't gotten much good news. HIV has outsmarted science.Until now. For the first time in the 14-year history of this fatal disease, mighty new antivirals are reducing the virus in a person's bloodstream to such low levels that current blood tests can't even detect the virus in a sample. The Food and Drug Administration has released three of these new antivirals, or protease inhibitors, so named for the way they inhibit a dreaded enzyme crucial to the life cycle of HIV.Although profound questions remain about the drugs' long-term efficacy -- as well as their skyrocketing costs and sometimes ruthless toxicity -- people living with HIV can now select from the strongest medical arsenal to date, and can obtain invaluable information about their own progress using new blood tests that measure the presence of the virus more accurately than ever.We have entered a critical moment in the history of the AIDS epidemic. Anecdotally at least, many people seem to be getting better. In L.A., dozens of once-ill patients like Eastman and psychotherapist Bruce Fitzgerald are enjoying unexpected new well-being. In some cases, PWAs have beaten, at least for now, the pernicious opportunistic infections that plague those with poor immunity, such as skin diseases, pneumonia and fungal assaults. Curing a lesion may not sound like the magic bullet for which everyone has yearned, but in the world of immunology, it's a big step forward."We should be dancing in the streets," says Dr. Farthing, a noted L.A. AIDS researcher and clinician. "We may in fact eradicate HIV from the bodies of some of the more fortunate patients." Dr. David Ho, a leading AIDS researcher in New York, speaks of "remission" as an option in the near future. At one L.A. meeting, he even dared to use the dreaded four-letter word, cure.Most doctors don't promise anything yet. No studies indicate a "cure." However, they do show sharp reductions in viral load -- meaning the number of viruses found in the bloodstream -- and an increase in the number of disease-fighting white blood cells, known as T-helper cells (or CD4 cells)."I don't even feed them lines about feeling better," says Dr. Christopher Ried, an AIDS physician in L.A. who has placed 80 percent of his patients on a protease regimen. "Maybe just an improvement in viral load." But he has seen viral loads plummet from 100,000 to 1,000, and concedes, "It's exciting for an AIDS doc in 1996 to take a patient who's had zero T-cells over the last four years and take him to 100. Patients who were ready to die are suddenly not dying."Indeed, at a time when scientists have learned not to overstate the case for medical answers to AIDS for fear of creating a new round of tragic false hopes, even cautious researchers and physicians are beginning to use guarded superlatives:"We may be close to achieving almost total suppression of the AIDS virus in most patients," says Dr. Emilio Emini, executive director of the antiviral research division of Merck & Co., which makes indinavir, also known as Crixivan. In a Washington, D.C., speech last January to the Third Conference on Retroviruses and Opportunistic Infections, Emini said the virus couldn't be found in the blood of 85 percent of patients who took a protease inhibitor along with two other antivirals."The new drugs are at least tenfold more potent than drugs we've been using for the last nine years," says Robert T. Schooley, M.D., of the University of Colorado Health Sciences Center in Denver, who chaired the conference's scientific program committee."The effect is more powerful than many would have dreamed possible when the studies began only a few months ago," reported a February 6 New York Times front-page story, predicting that HIV will soon be treated as a chronic incurable disease, like diabetes.The jury's still out on such predictions. No one knows how long these drugs will suppress the virus or who will pay for the therapy, which can run from $12,000 to $18,000 a year. To remain effective, protease inhibitors need to be taken along with old-fashioned antivirals (known as reverse transcriptase inhibitors). These "drug cocktails," plus new, high-tech blood tests that precisely measure viral activity, have jacked up an already high price tag.Indeed, warn some activists, before counting your change, keep in mind that most data from studies are preliminary and too new to have been replicated. So much is still unknown. Should protease therapy begin when patients are newly infected but healthy, or when their immune systems are shot? Researchers warn of cross-resistances that develop between one protease inhibitor and another. Patients like L.A. city AIDS coordinator Ferd Eggan warn of occasional side effects worse than the disease itself. A minority of patients (15 percent) experience nausea, and even fewer experience elevated triglycerides and kidney stones. Some have questions about the viability of the clinical trials: In what stage of development is a given drug? How many people have taken the drug? At what stage of infection have people been studied? What populations have been studied?Dr. Ried questions whether T-cells that are regained by PWAs taking protease are as powerful as the T-cells they lost. "I'm not sure if the new T-cells have the memory to fight off cytomegalovirus or cryptosporidum, the nasty things you get when you have 50 T-cells or less," he says. And most problematic of all, if patients don't take protease inhibitors religiously and on schedule, they can foster resistant strains of HIV that make sick people even worse. Once you start on protease, you should never stop, because "You induce resistances, and those resistances then take over and the drug can't touch them," explains Dr. Scott Hitt of the Pacific Oaks Medical Group. But given the sometimes vile side effects of these drugs, such as nausea and diarrhea, lifelong therapy is no picnic. And what if HIV isn't the main cause of AIDS -- a question still brewing in radical segments of the scientific and AIDS-activist communities?No wonder the AIDS community isn't dancing in the street. All the same, many are growing deeply curious.At the Community Forum on Protease in April at Paramount Studios, Los Angeles, 700 or so men and women in all stages of HIV disease crowded into an auditorium. They included the worried well, the blind, people wearing catheters, people using canes, and even some who were carried in by lovers or mothers.The presentation, organized by Jules Levin of the National AIDS Treatment Advocacy Project, couldn't have been more scientific. Representatives of the five major HIV protease-inhibitor manufacturing companies had been invited by New York's Levin to present the basic science on their drugs. Despite the medical jargon ("The maximum median viral load decline with saquinavir/AZT was 1.6 logs after two weeks," explained one researcher), they had a rapt audience.Richard Cooper, an L.A. AIDS physician, explained that protease inhibitors differ dramatically from other available anti-HIV drugs, such as AZT, ddI, ddC, d4T and 3TC. They work at a later stage in HIV's replication process, when HIV has already entered the cell's nucleus and made long chains of proteins and enzymes that will form many viable copies of HIV.Scientists now know that these chains do not have the ability to wreak havoc until they are cut up into smaller pieces by the dreaded HIV protease enzyme, which acts like a chemical scissors that frees HIV to begin its destructive work.The new protease inhibitor, an elegantly engineered molecule, has been designed to stop that snipping and replicating process. The inhibitor is welcomed into infected cells like a Trojan horse, and then essentially "gums up" the nasty chemical scissors -- inhibits them -- preventing the protease enzyme from being divvied up and thus making new copies of itself and of HIV.Three FDA-approved protease inhibitors -- saquinavir, ritonavir, indinavir -- and others now being studied, such as nelfinavir, all work by gumming up the scissors. But they differ dramatically in how they affect the body and how often they must be taken. Some are more potent than others, but all must be taken daily and at specific intervals. Unlike the old approach with AZT, patients are urged not to take a break from protease inhibitors ever, because the surviving HIV strains that are resisting the protease inhibitor will rapidly overtake the body.But the regimen might be worthwhile. In the 1995 trial of 1,200 patients in 67 centers in the United States, Canada, Europe and Australia, researchers found that the protease inhibitor ritonavir nearly halved the death rate and the appearance of new AIDS-related complications in severely ill patients. In another study summarized by Dr. Trip Gulick at last January's retroviral conference, 90 percent of the 26 patients receiving a triple-drug combination (indinavir, AZT and 3TC) experienced such a huge drop in their viral load after four months that the virus could not be detected. Dozens of additional studies confirm similar good news.Studies also document, though, that the drugs make a minority of patients feel sicker than they are. Ritonavir, approved in March, perhaps the most powerful inhibitor, also produces the most acute side effects. It can in some cases elevate nausea and cholesterol in an alarming manner. Viracept, still in clinical trials, can cause chronic diarrhea. Indinavir, which was approved by the FDA in April, causes kidney stones in 2 to 3 percent of patients. Saquinavir, which was approved last December, must be taken with fatty foods but is less noxious than other protease inhibitors.At the forum, doctors representing the key drug companies (Abbott Laboratories, Agouron Pharmaceuticals, Glaxo Wellcome, Hoffmann-La Roche, Merck Research Laboratories and Vertex Pharmaceuticals) presented the stringent "do's and don'ts" on specific protease inhibitors. All of these drugs are so powerful, and sometimes so hard to digest, that a person may need to try more than one before "clicking."But once a drug does click, patients who fail to take it religiously run a great risk of developing resistance to one protease enzyme as well as to many others. HIV can change its chemical structure in order to resist the effects of drugs, and cross-resistance can occur when HIV becomes resistant to two or more drugs at the same time. For this reason, experts say, people taking AZT (a reverse transcriptase inhibitor) who also try a protease inhibitor should couple it with an additional reverse transcriptase inhibitor (ddC or ddI) they've never taken before and thus aren't resistant to. At a certain point, however, such options decrease."Because of all the uncertainties," says forum organizer Levin, "some physicians advise individuals to consider delaying making a treatment decision until more data are in. However, at a recent Washington [D.C.] conference, some AIDS researchers recommended treatment intervention as early as possible, with multidrug combination including a protease inhibitor."Despite the contradictory advice, Levin sounds an optimistic note. Soon, he says, PWAs will live longer, illnesses will be managed better, and a new technology of disease monitoring will emerge. And so, perhaps, will tentative hope. But Levin also confesses that, as in all matters relating to HIV, there's a lot of political dissension, a great deal of uncertainty, a fair amount of profiteering and tremendous disagreement among advocates themselves.Levin suffered his share of angry dissenters at the April forum gathering, for example -- men and women who complained that the new drugs were fancy kinds of rat poison. "More crap," one insisted."The forum made me feel very hopeful and really consider taking the drugs," said author and editor Mark Thompson. "It also made me realize that with every advance or leap, there's a shadow side. I don't know what the downside is yet, and I don't think the scientists do either."As usual, the AIDS community is split -- this time between antiviral advocates and antiviral nihilists.Dr. Charles Farthing looks like an English socialist with a stethoscope. His scrappy hair and tangled tie mark a sharp departure from the world of glitzy gay docs and power-suited researchers. He arrived in L.A. last year from New Zealand to become medical director of AIDS Healthcare Foundation, the largest community-run AIDS medical facility in the country. He is bullish over the current paradigm shift, which, as he explains it, has a lot more going for it than just new drugs.Two new viral-load blood tests -- called PCR and B-DNA tests -- allow doctors to measure the precise course HIV is taking in the body as never before. Previously, the only way to measure HIV disease progression was through counting "surrogate markers" -- the T-helper cells that indicate the number of healthy white blood cells. It is a less direct process in which a normal CD4 count is considered to be above 500. The Centers for Disease Control define clinical AIDS as a CD4 count below 200.But now, the precise number of viral RNA genes in a person's blood can be determined. Given the more sophisticated technology, the system of measurement will most certainly begin to focus as much on determining the exact viral load as on assessing the CD4 count.Because the level of RNA viral genes associated with increased risk of disease progression is thought to be between 100,000 and 200,000 copies per milliliter of blood, the new test not only helps a doctor decide when a patient ought to begin aggressive protease-inhibitor therapy, it also effectively measures the antiviral effect of the drugs being studied.This is unprecedented. In the past, according to Farthing, when patients with high T-cells appeared stabilized, it was believed that they were undergoing a latency period. "Now we realize that the virus was anything but latent," says Farthing. "Their bodies were manufacturing millions of copies of virus each day. About 2 billion T-cells are being produced and destroyed each day."This is very scary news, for it suggests that, from day one of infection, HIV undergoes a dynamic process in which a person's immune system is under constant, incredible siege. Like other viruses, HIV depends on the cells it infects to make new copies of itself, and these new copies infect other cells. One of HIV's favorite targets is the T-helper cell, or CD4 cell. When too many of these white blood cells are attacked, infections can occur. And that's when a person is said to have AIDS.HIV outsmarts infected cells that would normally resist an attacker by changing its RNA into DNA, then back to RNA. Until now, AIDS drugs like AZT attacked the beginning stage of the HIV life cycle. Known as reverse transcriptase inhibitors, those drugs were designed to disrupt the work of HIV enzymes called reverse transcriptase, which act to change HIV's chemical or genetic message into a form that can easily be inserted into the nucleus of a human cell.In the past, AZT therapy worked only for a period of a year or so. Then mutant strains of virus would take over, in a natural-selection process. Findings from a three-year study concluded in 1993 showed that HIV patients who began taking AZT in the early, asymptomatic stages of infection lived no longer than those who began treatment later, at the onset of AIDS. This was very disheartening news, suggesting the severe limitations of AZT.The new drugs can reduce the viral load in some people by 99 percent, but some infected dormant cells will survive. That's why combination therapies are being further investigated. Adding a protease inhibitor to AZT (plus one other reverse transcriptase inhibitor) means that HIV will get hit at two places in its replication cycle, the beginning and the end.Unlike AZT, which was designed to fight cancer, protease inhibitors are the first antivirals specifically engineered to combat HIV. And while resistant mutants can certainly remain viable even in the presence of the most potent protease inhibitors, the likelihood of the virus resisting two or three antivirals at once is remote. According to Australia's Dr. David A. Cooper, protease inhibitors represent the "demise of monotherapy." In Richard Eastman's case, for example, it was the "magic cocktail" of AZT, 3TC and ritonavir that finally worked. He's gained weight, is free of infections, and is enjoying a normal level of energy at long last. "Once, I felt that I had only months to live," he says. "Now, I measure life expectancy in years."Dr. Farthing says several studies show that multidrug therapies which include a protease inhibitor are likely to delay the emergence of drug-resistant variants of AIDS. That means the benefits are cumulative, because fewer viruses will be produced in the body, more healthy CD4 cells will thrive, and the person will get better and better. "Sure," Dr. Farthing says, "a patient may have to take dozens of pills a day (ritonavir plus AZT plus 3TC, let's say). But if he or she can tolerate the regimen, disease progression may indeed stop."To Farthing and many others, patient compliance is the biggest problem in the new world of AIDS medicine."It's going to be hard to convince a healthy HIV-infected man or woman to take these drugs that may make him or her feel quite nauseated at first when they feel healthy and vital now. The incentive is lacking to start a difficult routine. To make matters worse, we have a community that is very shy of medical therapy, especially given the very bad rap most drugs have gotten. But two or three years down the road, this healthy HIV-infected person may grow quite sick. We have to tell them that a little nausea now is better than death down the line. We have to develop a new way of talking about drugs and medicine, because we have something now that really works."Bruce Fitzgerald is an openly gay L.A.-based psychotherapist who asks that his real name not be used because he's concerned that his dramatic medical battle could upset his troubled clients. His adventure with protease inhibitors illustrates why people are both so excited and so depressed about the advances.Fitzgerald found out that he was positive in 1988 although his lover, Alan, was negative. (They have been together since 1983). He fell into depression and went into therapy. He tried no drugs, because he was asymptomatic, a common approach among those with HIV. When his T-cells dipped in 1992, he went on AZT. In June of 1993, he experienced his first two opportunistic infections -- cryptosporidium, which causes severe diarrhea, and eosinophilic folliculitis, known as "itchy bump disease."Fitzgerald knows about commitment. "They call me the Pill Queen in my support groups," he jokes. He attacked the virus through a variety of strategies including acupuncture, psychotherapy, couples counseling, dermatology and endless doctor appointments, and finally got his infections largely under control.When Hoffmann-La Roche began testing saquinavir through UCLA in the fall of 1994, Fitzgerald didn't think twice about entering the blind study -- even though he had to stop taking all antivirals and understood he wouldn't be told if he was really getting the protease inhibitor or just a placebo.Like many people who go off AZT to take a protease inhibitor, however, Fitzgerald underwent serious psychological fallout. Because protease inhibitors mark the last chance to stay alive, and one can never safely stop taking them or even miss one dosage, some takers are concerned because doctors don't provide much psychological support.Says L.A. writer Mark Thompson, "You just get the pills and are told to go home and take them like a good boy -- and don't you dare skip a dosage! -- and no one says a word about depression, despair, fear of failure, anxiety, panic attacks." Thompson even wonders whether "there isn't something about the substances themselves that aren't physiologically depressing. I frequently wake up feeling rotten. Once I get going, I don't notice it, but mornings are bad for me."Mornings have certainly been hell for Fitzgerald. By February 1996, he was so down and exhausted that he left the study to take norvir, but his viral load skyrocketed. After seven weeks, Fitzgerald knew he had to find a more effective protease inhibitor.He settled on indinavir (Crixivan), produced by Merck. Studies of indinavir prescribed alone, with a lower-than-recommended dose, have demonstrated a greater than 90 percent decline in viral load, as determined by the amount of HIV RNA in the blood serum. Studies also have shown a 50 to 80 percent increase in CD4 cells. One 24-week study of combined indinavir and AZT showed some patients experiencing a 99 percent decline in HIV RNA. In that encouraging study, a very low level of drug-resistant HIV developed.In other words, indinavir sounded like a damn strong strategy for a dying man. But Fitzgerald was told the drug wouldn't be available for six more weeks. Knowing how many billions of copies HIV could make in his body each day, Fitzgerald quickly decided to take ritonavir (sold as Norvir), one of Abbott's HIV protease inhibitors.Ritonavir must be eaten with food -- the fattier, the better -- and that diet was in keeping with Fitzgerald's high-calorie strategy to fight weight loss. Yet in retrospect, he says, "I would have preferred indinavir," even though it must be taken on an empty stomach, and no food can be eaten an hour before and two hours after the dose. (Today, docters permit a light meal.)The problem with ritonavir is its incredible side effects in a small percentage of patients. "After the first dosages," Fitzgerald recalls, "which took place seven weeks ago, I thought I was going to die -- literally." For the first three days, he experienced skin hypersensitivity, as if his entire body had been badly sunburned, with a cold throbbing in his sinuses. "If I took a finger and ran it down my neck, it would feel as if someone took a hot poker and seared my flesh with it. I literally didn't want to be touched, even though I felt so sad and down."This rarely seen sensation lasted until he changed his dosage from two times a day to three a day taking the same amount, but in smaller doses.In the end, Norvir turned out to be a terrible choice for him. His viral load, instead of dropping, skyrocketed. But that wasn't the only problem. Fitzgerald suffered severe flulike symptoms and difficulty concentrating. "I had some difficulty hanging in there," he recalls. "I thought I had reached a dead end." Luckily, Crixivan became available after he'd been on Norvir seven weeks, and Fitzgerald made the switch to Crixivan three weeks ago. Whether Crixivan is reducing his viral load is unknown -- tests typically aren't taken until a month into treatment. Despite the numerous setbacks, Fitzgerald holds out hope that he can grab a few more years of life, until the next generation of drugs is released. "It's an exciting time to be alive," Fitzgerald says. "I'm keeping my fingers crossed. It is a lot of work and such a leap of faith to go with something when the results are so fuzzy. I'm hoping the Crixivan is effective in reducing my viral load. If it doesn't work, there's still another one coming out soon -- Agouran -- and I've heard there's yet another new AZT-type of drug coming out too. There are lots of reasons to maintain hope and hang in there."But Fitzgerald is a white, middle-class gay professional with a devoted "husband" and a disability plan that allows him to work half time. He has the skills necessary to be a successful protease-inhibitor taker: organization, discipline, deferring pleasure for reality. It's not at all clear, however, whether most of the people dealing with HIV infection will be so lucky, attentive or supported.On April 18, employees of Stadtlanders Pharmacy and Wellness Center arrived at their downtown Manhattan offices to find the plate-glass window covered with graffiti assailing them as "Profiteers" and "Price Gougers." It was quintessential ACT UP. The direct-action street group was protesting Stadtlanders' role in distributing indinavir, a protease inhibitor created by the giant Merck & Co.Merck had given Stadtlanders an eight-month monopoly on indinavir sales, which allowed the latter to profit from a 37 percent markup.In fact, the entities who stand to benefit most from the new advances in AIDS research are the pharmaceutical manufacturers. They, for the first time, can treat HIV as a chronic condition that requires patients to take drugs over the course of what many believe could be a normal life span. The market for HIV drugs could top $3 billion in the next few years. Who will check this unbridled capitalism?Unfortunately, the AIDS-activist community isn't as galvanized as it was during the release of AZT in 1987, when activists swarmed the FDA and pummeled Burroughs-Wellcome with demands to lower costs. ACT UP has lost hundreds of its once-obnoxious foot soldiers to AIDS. Many others have left the streets to work within the AIDS industry as publicists, bureaucrats and lobbyists.At the same time, the drug-assistance program authorized under the federally funded Ryan White Act is nearly broke in California. As doctors face pressure to treat HIV patients earlier in the course of infection and with multiple therapies, it's not clear how private insurance will react, especially when some drugs are still experimental. The $200 viral-load tests, for example, aren't FDA-approved, and Medi-Cal won't pay for them.What an odd irony of fate. Just as the options have expanded for AIDS treatment, budget cuts on the state and federal levels put such drugs out of reach of anyone not filthy rich.Everyone stands to lose, however, if too many financial resources are squandered or withheld. Money is needed not just to deliver drugs to middle- and lower-income populations, but also to continue to craft well-designed clinical trials to test old and new drugs.In addition, too many important questions must be answered before too many people rush to their doctors for help: Should treatment start soon after HIV is detected, or not until a person shows high viral activity? Would certain types of infected people benefit from watchful waiting? Just how do HIV mutations develop in response to each drug? Is it effective to take more than two protease inhibitors along with two older drugs? How much of each drug should be used in a combination? Will a low dosage create resistant strains of HIV? Will a high dosage make people too sick to want to live?The answers lie not just in the hands of medical experts or with heads of pharmaceutical companies, but in the lay members of the AIDS community itself. As past experiences with older AIDS drugs have demonstrated, AIDS activists have at least some power to see that drugs are delivered quickly and fairly.But some activists see a real malaise blanketing the worn-out AIDS community. Some even conjecture that the community entertains, if not a death wish, an existential identification with the current suffering.Andrew Sullivan, author of Virtually Normal, suggested in an editorial in The New Republic that gay people are no different from the survivors at the end of Camus' The Plague. When the gates of the quarantined city finally opened, people were terrified of leaving."I wonder if people will feel they have a purpose in life if AIDS is no longer deadly," worries AIDS Healthcare president Michael Weinstein. "We went from a magnifying glass to an electron microscope in terms of AIDS care. We went from being gravediggers to lifesavers." Yet, he says, "Most people aren't talking about this as a new moment of hope and change."It may take time before hundreds of thousands of infected people feel motivated enough to try the new drugs. The same holds true for the hundreds of thousands who suspect they are infected -- estimated to be half of the infected community -- but are too pessimistic to take the HIV-antibody test. AIDS-prevention activists argue that better drugs may increase the incentive to find out one's HIV status. But so far, the masses aren't rushing to the testing sites.It'll take more than curiosity. To make protease inhibitors work, a new system of care must be created that includes specialized clinics for the homeless as well as the white-collar PWA, where clients are aggressively monitored and supported while taking these sometimes difficult new drugs. Even as AIDS spreads through society, new ways to follow up on care, and to deliver drugs, need to be devised.A conversation among PWAs, activists, doctors, CEOs, researchers and psychologists certainly needs to take place. But there is no precedent for such a dialogue. So much depends on the level of urgency people feel and how motivated they are. There is still no cure for AIDS, and that's depressing. But top scientists and people with AIDS like Richard Eastman and Bruce Fitzgerald are talking seriously about HIV no longer being absolutely fatal. And that's the beginning of a change. And maybe hope.

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