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AIDS Treatment News
September 29, 1995

Contents:

  1. ICAAC 1995: New Perspectives on Treatment
  2. Major Study Shows AZT Monotherapy Inferior
  3. Abbott Protease Inhibitor In Combination: Sustained Viral Load Drop
  4. Agouron Protease Inhibitor
  5. Saquinavir (Roche Protease Inhibitor) At Higher Doses
  6. Ritonavir, Saquinavir Combination -- and Warning
  7. Symptom-Reduction Trials at FDA Clinical Trials Workshop
  8. Medicaid in Congress: Serious Threat to Health Care

ICAAC 1995: 
New Perspectives on Treatment

by John S. James
Most AIDS conferences leave a sense of disappointment, of how little new or significant work has been done. But ICAAC 1995 -- the 35th annual Inter-Science Conference on Antimicrobial Agents and Chemotherapy, in San Francisco September 17-20 -- was clearly different -- and important. ICAAC focuses on new antibiotics for all infectious diseases -- perhaps a fifth of the 1800 presentations were relevant to AIDS -- but the 1995 meeting was especially necessary since the International Conference on AIDS has begun a two-year schedule and, for he first time, will not occur this year. ICAAC was pivotal not so much for the meeting itself (and certainly not for how the meeting was administered), but as a marker of far-reaching changes which were already happening. The conference included important new information, and it brought key people together, allowing new thinking and new controversies to be more readily grasped.

Treatment information is changing rapidly, and experts often disagree on what it means. Anything we say may soon be obsolete -- even as soon as next week (after the Fifth European Conference on Clinical Aspects and Treatment of HIV Infection, September 27-29 in Copenhagen). Readers should note that what we report is not established truth, but rather a collection of theories or views which may -- or may not -- prove helpful for understanding AIDS treatment developments. Remember that this article was written in late September 1995; next month or next year the picture will be different.

Since we must be selective in reporting hundreds of research presentations and what people are saying about them, readers should know what our emphases and/or biases are:
  • As a result of ICAAC, we have come to believe that the single most important research direction now is to test protease inhibitors in patients, in the most promising combinations -- both with other protease inhibitors, and with other kinds of treatments for HIV disease. Instead of trying less promising combinations first, as has often been done in the past, we should move straight to the best ones which are in view. The trials required can usually be small, fairly simple, and inexpensive; they can report results in weeks or months, although long-term followup will be needed in addition. The main obstacles to running these trials are organizational -- especially in getting different pharmaceutical companies to work together. As researchers learn what the drugs can do at their best, they can also learn how to deliver the best possible care under real-world constraints.

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  • The most important immediate result of new information released at ICAAC (and the major conference the following week in Copenhagen) will be that the current "standard of care" that most treated patients receive today -- starting with AZT alone -- will go away. Instead, physicians will use combinations (often including AZT), and they will have a menu of possible treatment choices, with little data to prove which choice is best on the average. This situation will greatly increase the need for practical guidance on how to individualize patient care -- for example, by using viral load, CD4 count, and other tests to tell when a regimen is not working, so that a different regimen can be tried instead.

  • Treatment failure -- especially but not only the development of drug resistance by HIV -- will become more central, since physicians will need guidance on planning sequences of treatments to minimize these problems.

Several of the following articles focus on the single most important session of ICAAC 1995, the "late breaker" meeting on September 18. Late breakers are research reports which arrived too late for the regular program, but were important enough to be included anyway; in recent years some conferences have set aside a special session for this purpose. Of 80 papers submitted for this late-breaker section, only 10 were accepted, because of limited time in the program; the others are unlikely to see the light of day at least until the Human Retroviruses conference in early 1996 (journal publication would usually take even longer than that).

We also cover one of the reports not accepted for the late breakers ("Protease Inhibitor in Combination -- Sustained Viral Load Drop," below), since it is particularly important, and the principal investigator was willing to share it with us.

[Scientists in many fields are now doing much of their professional communication on the Internet -- publishing their results, organizing their own peer review when necessary. Because it is immediate, the Internet establishes better proof than journal publication of who originated an idea; at the same time, it makes the latest work available almost anywhere throughout the world, allowing feedback and participation regardless of location. Scientists and scholars can be free of the arbitrariness of journals and conferences, no longer required to keep their work secret for months or years of unnatural delay, able to communicate freely without regard to publication schedules, limited time in meeting halls, or professional rivalries and gamesmanship.

For the Internet to catch on as a mainstream professional forum, it needs enough critical mass of colleagues using it in this way. In AIDS, most researchers do use email at this time; but the momentum for widespread initial publication of original AIDS research on the Internet has not yet developed. When it does, everyone will benefit.]


Major Study Shows 
AZT Monotherapy Inferior

by John S. James
A major government study has found that AZT alone was inferior to AZT plus ddC or AZT plus ddI combination therapy, or to ddI alone, in patients starting with a CD4 (T-helper) count between 200 and 500. This finding, first reported in the press on September 14 and later described in more detail in a preliminary analysis at the ICAAC conference in San Francisco, is expected to change the common practice of putting people on AZT alone as their first treatment for HIV infection.

[Note: As this issue went to press, we learned that the results of another major AIDS trial, the Delta study in Europe and Australia, strongly confirmed the ACTG 175 results, showing that AZT plus ddC or AZT plus ddI had a substantial survival benefit over AZT alone. The Delta study did not have a ddI-only treatment arm. The Delta researchers strongly recommended that when people first start anti-HIV therapy, they use one of these combinations instead of AZT alone.]

The U.S. study, called ACTG 175, enrolled over 2,000 volunteers and lasted for two years. It randomly assigned patients to receive one of four treatments:
  • AZT alone,
  • ddI alone,
  • AZT plus ddI,
  • or AZT plus ddC.

It looked primarily for three different outcomes:

  1. survival;
  2. a clinical endpoint consisting of either progression to AIDS or death; or
  3. a 50% or greater drop in CD4 count (or progression to AIDS, or death, in case they occurred first).

If somebody did poorly (either because they developed an AIDS-related condition, or because their CD4 count fell by 50% or more) they were switched to a different study regimen which might be more beneficial -- those on single-drug therapy being switched to the combination, and those on one of the combinations being switched to the other one. In addition, several substudies were "nested" in ACTG 175, to test some of the volunteers more thoroughly in order to answer specific questions. A virology substudy measured viral load from over 300 of the volunteers, at intervals of 8, 20, 56, 80, and 104 weeks; these data have just begun to be analyzed (see "ACTG 175 Viral Load Substudy," below).

Other substudies include pharmacology, women's health, and quality of life; these have not yet been analyzed, however. About half of the volunteers discontinued their medications before the end of ACTG 175. Only seven percent of these discontinuations were mandated by the protocol, due to severe adverse experiences which were considered to be possibly drug related. Others discontinued for different reasons such as milder adverse events, disease progression including CD4 decline, or the large number of pills which needed to be taken (because the study was blinded, everyone had to take pills for all three of the drugs).

Those in the ddI-only arm discontinued less often than those in other arms. Fortunately, most of those who discontinued taking their protocol-specified medications still remained in the study for followup purposes. 19 percent of the volunteers in ACTG 175 were lost to followup by December 1, 1994.

[Statistical note: In the presentation of the clinical results of ACTG 175, distributed as a 49-page executive summary, the data were analyzed by the "intent to treat" method. This means that the patients were averaged based on the medication which they were randomly assigned -- even if they changed that medication later. Intent to treat analysis has certain advantages for statistical interpretation -- and certain disadvantages as well. In this case, an exception to strict intent-to-treat rules was made, in that patients who NEVER took their assigned medication were excluded from the analysis.]

Overall Results of ACTG 175

The most important results were found by separate analysis of the "antiretroviral-naive" and "antiretroviral-experienced" volunteers. The antiretroviral-naive group had never received AZT, ddI, ddC, or other antiretrovirals -- or had taken such treatment for less than a week. The "antiretroviral- experienced" volunteers had been heavily treated with AZT before the study began; 42% had already taken antiretrovirals (almost always AZT) for two years or more, and another 24% had been treated for more than one but less than two years.

Results for Those Starting Antiretrovirals

For those who had not taken antiretrovirals before, the death rate during the trial was 7% for those who started AZT alone -- compared to 4% for ddI alone, 4% for AZT plus ddI, and 3% for AZT plus ddC. (This difference is not statistically significant, however, meaning that it could well have happened by chance alone -- since not many people died.) For the same patients, the rate of either progressing to AIDS or dying during the trial was 12% for those starting on AZT alone, vs. 9% for ddI alone, 8% for AZT plus ddI, and 6% for AZT plus ddC. (Only the difference between AZT alone and AZT plus ddC is statistically significant here.) And for these patients, the rate of progressing to either a 50% or greater CD4 count decline or AIDS or death, was 23% for AZT alone, vs. 17% for ddI alone, 14% for AZT plus ddI, and 10% for AZT plus ddC. (Here, all the comparisons between AZT and the other three treatments are statistically significant, as is the comparison between ddI and AZT plus ddC.)

These data clearly suggest that AZT alone is worse than the other three regimens as initial therapy, in the patient group studied in this trial. AZT plus ddC may have performed best of the four regimens, but it is impossible to be sure of that from the data.

Results for Those Previously Treated with AZT

For the antiretroviral experienced group, the comparable results are as follows: The death rate during the trial was 10% for those taking AZT alone -- compared to 5% for ddI alone, 6% for AZT plus ddI, and 9% for AZT plus ddC. (The differences between AZT vs. ddI, and AZT vs. AZT plus ddI, are statistically significant; the other comparisons are not.) The rate of either progressing to AIDS or dying during the trial was 18% for those using AZT alone, vs. 14% for ddI alone, 13% for AZT plus ddI, and 17% for AZT plus ddC. (Only the difference between AZT alone and AZT plus ddI is statistically significant.) And the rate of progressing to either a 50% or greater CD4 count decline or AIDS or death, was 38% for AZT alone, vs. 26% for ddI alone, 22% for AZT plus ddI, and 27% for AZT plus ddC. (Here, all the comparisons between AZT and the other three treatments are statistically significant.) So AZT alone was also worse than the other three regimens for those who had already taken AZT. AZT plus ddC did relatively poorly for those who had already taken AZT (especially in the clinical endpoints, AIDS and death), although it did not do as badly as AZT alone.

The ACTG 175 Virology Substudy

Viral-load results of ACTG 175 were not included in the executive summary. Instead, a preliminary analysis was quickly put together for the ICAAC late-breaker session. Viral load was not measured on everybody in ACTG 175, but on a selection of the volunteers; 196 of them were antiretroviral naive, and 152 were experienced. Viral-load samples were taken twice at baseline, and at 8, 20, 56, 80, and 104 weeks. The amount of virus will be measured by several different methods, but only plasma HIV RNA has been analyzed so far, and is described here. Overall, viral load showed a much smaller decline from the AZT-only treatment than from the other three treatment regimens. By eight weeks, the viral load had already predicted the main conclusion of the two-year study -- that treatment with AZT alone was inferior to the other regimens. The viral load averages at 80 and especially at 104 weeks were less reliable than at earlier times because of drop-outs from the trial, and also because changes of study medication. (Viral load samples were included in the analysis presented at the late-breaker session only if patients were still on the treatment to which they were assigned; this is different from the "intent to treat" analysis used for the clinical outcomes of ACTG 175, described above). Therefore, the descriptions below apply to the baseline and the first three time points unless otherwise noted.

For the antiviral naive patients, the two combination treatments were most effective in reducing viral load, with AZT plus ddC perhaps being a little better on the whole than AZT plus ddI, although they are close enough that it is not possible to tell for sure. ddI alone was intermediate between AZT alone and the two combination treatments. For antiretroviral experienced patients, AZT again was clearly the least effective in lowering viral load; in fact, it did not lower viral load at all. The other three treatments were about equivalent to each other in the experienced patients. Overall, each of the two combinations showed about a 0.7 log (5-fold) decrease in viral load, sustained for the first year of the study. (After the first year, there may have been some drop-off in viral suppression, but it is hard to be sure because of the small number of samples left after patients dropped out or changed medications, as mentioned above.)

The viral-load results we most want to see from ACTG 175 would not be group averages, but a patient-by-patient analysis of how to use viral load, and short-term changes in viral load after starting therapy, to predict the risk of long-term clinical progression if treatment is not changed. This information is not yet available.


Abbott Protease Inhibitor 
In Combination: 
Sustained Viral Load Drop

A clinical trial in France with about 25 volunteers combined ritonavir (the Abbott protease inhibitor) with AZT plus ddC, in patients who previously were untreated. The combination achieved a 2.5 log (more than 300-fold) average drop in HIV viral load, as measured both by HIV RNA and by infectious virus; this drop has been sustained for 20 weeks so far and is still continuing. This result was submitted by Jacques Leibowitch, M.D., a clinical immunologist at the Raymond- Poincare Hospital/University Rene-Descartes, Paris Ouest; it was apparently too late even for the late-breaker session, but a couple of Dr. Leibowitch's slides were shown in a late breaker presentation from Abbott Laboratories. And Dr. Leibowitch showed us some of his other slides when we met in the aisle during the conference.

The proportion of patients with at least a 99.9% drop in viral load has kept increasing over the five months of this trial, and has now reached over 50%. We need to learn more details of this study. The continuing increase in the proportion of patients who respond very well to this treatment suggests that immune-system recovery may be helping the drugs to control the virus. If so, effective viral suppression might be sustained for a long time.

At the ICAAC conference, there was much discussion and interest in combining a protease inhibitor (either ritonavir or one of the others) with combinations of other antiretrovirals, especially AZT plus 3TC, or AZT plus ddC. There is nothing magic about these particular combinations, however; the goal is to get good viral suppression in addition to the suppression due to the protease inhibitors. For persons who have already used AZT for a long time, effective combinations of other drugs which they have not used might work better. This strategy needs more attention and research.

[Note: A larger trial, ACTG 229, combined a different protease inhibitor (saquinavir, developed by Hoffmann-La Roche) with AZT plus ddC. Viral suppression with the triple combination was better than in the other arms of that trial, but not nearly as good as in the new French study. The difference in results may be because patients in ACTG 229 had extensive prior use of AZT; all the volunteers had used it for at least four months, and most for more than a year. Also, ACTG 229 used a dose of saquinavir which many now suspect is less than the optimum dose.

[An Italian study found a 1.7 log (50-fold) viral load drop with the current dose and formulation of saquinavir, combined with AZT only. Hoffmann-La Roche is now conducting a major international study, which has already enrolled 2000 patients and will enroll 1000 more, which includes a treatment arm combining saquinavir, AZT, and ddC in AZT-naive patients.]

[Safety note: Ritonavir MUST NOT be combined with any of a number of other drugs, both common prescription medications and certain experimental treatments. Anyone using ritonavir -- which is not widely available -- must follow all instructions carefully.]


Agouron Protease Inhibitor

Agouron Pharmaceuticals, Inc. of La Jolla, California, is developing a protease inhibitor called AG 1343, trade name Viracept(TM). Two small studies, each checking the tolerability and antiviral activity of different doses of the drug, in slightly different formulations, were presented at the late breaker session at ICAAC. The first study, with 22 volunteers, was conducted in the UK; the second study, in the U.S., with 30 volunteers, tested higher doses.

The main results (from the two studies together) were:
  • The drug was well tolerated in all the doses tested. Some patients had small to moderate side effects, including diarrhea (which may have been due to the particular formulation of the capsules, which has been changed) and fatigue.

  • Almost everyone had good responses either in viral load reductions, or in CD4 count increases; however, there was often no clear relationship between these two responses. CD8 cell counts were also found to increase.
  • No clear dose-response relationship was found. But when blood levels were examined, those with higher levels of the drug had a more sustained response.

  • Average viral load changes could be as much as 1.5 logs (about 30-fold) at maximum. But a number of patients had less than a one-log drop in viral load at 28 days; in the larger of the two studies, they were dropped from the study at that point.

  • Both studies also noted improvement in clinical conditions, such as swollen lymph nodes, hairy leukoplakia, and folliculitis.


Saquinavir (Roche Protease Inhibitor) 
At Higher Doses

Saquinavir, a protease inhibitor developed by Hoffmann-La Roche, is currently in large-scale clinical trials at a dose of 1800 mg per day (600 mg three times a day).

[Recently a new formulation of the same drug has been developed to increase the low bioavailability of saquinavir (the low absorption into the bloodstream after the drug is taken orally); see the notice about the new saquinavir trial in this issue of AIDS Treatment News].

Meanwhile, a small (40- patient) study at Stanford University has tested higher doses of the original formulation, with intensive patient monitoring, to make sure that higher blood levels are safe, and do increase antiviral activity. Results of that study, which compared doses of 3600 and 7200 per day (twice and four times the dose used in other trials), were reported in the late-breaker session at ICAAC. Twenty patients with CD4 counts from 200 to 500 were given each of the doses. This trial lasted for 24 weeks. Both doses significantly decreased viral load and increased CD4 count. But the high dose resulted in greater and more sustained responses. This study also looked for two mutations in the virus which are critical in the development of resistance to this drug -- mutations at positions 48 and 90 of the HIV protease gene. These mutations developed more slowly in the high-dose arm, with four out of 19 patients having one of them when the study ended on week 24, compared to 9 patients out of 20 having a mutation with the low dose. No patient developed both mutations.

Some adverse effects were found, somewhat more at the higher dose; all resolved when the drug was discontinued. Only one patient, at the high dose, chose to discontinue the study, due to transient diarrhea and confusion. Three others (also on the higher dose) needed a brief drug holiday due to abnormalities in various blood tests (one for modest elevation of liver-function tests, one for increased CPK, and one for neutropenia); but these three were able to re-start and continue drug at the full dose. There were also some milder side effects, mostly at the high dose, but most patients finished the study without dose modification. The low-dose group had a maximum average CD4 increase of 72 at week 4; this increase declined and was only 31 at week 24. In the high-dose group, the CD4 count continued to rise until it reached an average increase of 121 at week 20; it was still 82 above baseline at week 24. The high-dose group had a maximum viral-load drop of 1.34 logs (22-fold), vs. 1.06 logs (11-fold) maximum drop for the low dose. At week 24, the high-dose group had an average reduction of 0.85 logs (7- fold) vs. 0.48 logs (3-fold) at week 24.

Some patients were also tested for the amount of drug in their blood (using the AUC, or area under the curve, measurement of blood levels). There was a clear relationship between higher AUC and greater drop in the viral load, with the higher dose clearly showing the greater drug levels. But there was considerable patient-to-patient variation in AUC within each dose level.


Ritonavir, Saquinavir Combination -- & Warning

Laboratory evidence suggests that two protease inhibitors, Abbott's ritonavir and Roche's saquinavir, might work particularly well together. (But caution: this combination will be very dangerous unless the dose of saquinavir is drastically reduced; since no one yet knows how much to reduce the dose, this must be tested in a carefully controlled study.) The possibility of combining the drugs was discussed by researchers from Abbott at the ICAAC late- breaker session.

The laboratory tests suggest two different rationales for research on this drug combination:
  1. HIV is known to develop resistance to all known protease inhibitors. But the initial mutations which confer resistance to ritonavir are different from the mutations which lead to saquinavir resistance.Therefore, combining the drugs may delay the development of resistance to both.

  2. An additional problem of saquinavir is that it is difficult to get adequate blood levels.

In tests in rat, combining saquinavir with ritonavir greatly helps to overcome this problem. The reason is that ritonavir blocks an enzyme which the liver uses to metabolize and eliminate saquinavir. (The same enzyme also metabolizes ritonavir itself; ritonavir has an unusually long half life in the body because it blocks this enzyme.) In tests in rats, combining the drugs increased the maximum blood concentration of saquinavir by 18-fold, and also greatly extended the time the drug was in the blood -- increasing total exposure to saquinavir by 290 times. Some researchers believe that the difference in humans, while still large, may not be that extreme.

Obviously it would be very dangerous to combine the drugs without reducing the saquinavir dose, because this would lead to a huge overdose of saquinavir. But properly managed combination use might be very beneficial -- especially since the main problem with saquinavir is getting enough of it into the blood. For the same reason, ritonavir MUST NOT be used with certain common drugs -- at least not unless the doses of those other drugs are properly adjusted. Anyone using ritonavir must be especially careful to follow medical advice.


Symptom-Reduction Trials 
at FDA Clinical Trials Workshop

by John S. James
At the FDA workshop on clinical trials (September 6 and 7, with associated meetings on September 8; see discussion in AIDS Treatment News #228 and #229), our major goal was to put our proposal for symptom-reduction trials onto the table for discussion. We were impressed with the openness of people to considering this kind of trial design -- not as something they necessarily agreed with, but as a possibility worth serious examination.

(For an earlier draft of our proposal, see AIDS Treatment News #229.) "Symptom reduction" trials is a name we used for a kind of trial in which everyone entering must have a certain, carefully chosen, "indicator symptom" -- a symptom or condition which is believed to be caused by immune deficiency or otherwise by HIV disease, and which is unlikely to resolve quickly on its own, or with conventional treatment. The trial then tests an antiviral drug (or an immune modulator, or other treatment for HIV disease) to see how well it works to make the symptom go away.

The major advantage of this kind of trial is that it tests for a CLINICAL BENEFIT of the proposed treatment (a concrete benefit to patients, not only a blood- test number), and yet it produces results RAPIDLY, since anecdotal reports suggest that many HIV-related symptoms can respond in days or weeks to effective treatment for HIV -- almost as fast as viral load responds.

Conventional AIDS/HIV clinical-benefit trials take the other approach, of measuring disease progression by waiting for new symptoms or conditions to appear. Since HIV disease develops slowly, and most patients will never contribute to the study result, this approach requires large, expensive trials that usually take years to organize and run.

Recently we learned that Abbott Laboratories has been exploring a symptom-reduction kind of trial design, independently of us, in an effort to find a faster way to get its protease inhibitor approved. And at the clinical-trials workshop we learned that the idea of using symptom reduction to tests antivirals has occurred to AIDS researchers over they years. But we do not know of any AIDS trial yet which screens for a specific symptom as an entry criterion -- a symptom NOT directly responsive to the drug being tested -- so that the symptom can indirectly indicate whether or not there is immune-system recovery due to the experimental treatment.

At the clinical-trials workshop, others suggested three important improvements to our proposal:
  1. We had divided clinical trials between those whose primary outcome is surrogate markers (such as viral load, or CD4 count), and those whose primary outcome is clinical. A better view is to distinguish three kinds of trials:
    • surrogate marker,
    • short-term clinical benefit, and
    • long-term studies (which examine benefits vs. side effects of drugs over a long time span, usually many years).

    Symptom-reduction trials produce clinical evidence, but not long-term results. (There is increasing agreement that long-term protocols are problematic -- that AIDS trials certainly need better long- term FOLLOWUP, but perhaps without requiring patients to stay on the same treatment or protocol for years.)

  2. A number of people proposed different indicator symptoms which might work better in drug trials than the ones we had suggested. Pediatricians thought that correcting growth failure in children would be an appropriate test for an anti- HIV treatment. Others suggested improvement in sinusitis.

  3. Statistician Andrew M. Hill, from Glaxo Research and Development Limited in the UK, suggested using viral load in addition to symptom reduction, and then doing a dose-response analysis -- seeing if patients with the biggest change in the "dose" of HIV also had the biggest reduction in symptoms. A related analysis might help to validate viral load as a proven "surrogate marker" of clinical improvement -- in a time frame of months, instead of the years which would be required for a trial to validate the marker as a surrogate for progression to AIDS.


Medicaid in Congress: 
Serious Threat to Health Care

Both houses of Congress are developing legislation which would greatly reduce Medicaid (Medi-Cal in California) coverage over the next seven years, and at the same time remove Federal standards for health care for the poor by converting the remaining Medicaid money into medical block grants that each state can spend as it likes. President Clinton might or might not veto these plans. Whether or not these proposals become law will depend on how much the public mobilizes against them.

These Medicaid changes are extremely serious for persons with HIV and other major illnesses. Medicaid is the only source of medical care for at least 40 percent of adults with AIDS; and 90 percent of children with AIDS also use Medicaid. According to the San Francisco AIDS Foundation, Medicaid provides approximately $3.5 billion in HIV/AIDS care -- six times the amount funded by the Ryan White CARE program. The National Association of People with AIDS, in a September 26 fax, called these Congressional Medicaid proposals "a train wreck that doesn't have to happen." AIDS Action Council, also on September 26, suggested that organizations approach their Congressional representatives, and also reach out to the press -- both the mainstream press, and also the community press, such as lesbian and gay, people of color, and women's weeklies, to document the human impact of these cuts and so-called "reforms." Also, an organization sign-on letter is available from any of the groups below.

How to Help

For more information about how you can help, contact the Coalition for Emergency Action on Medicaid Funding, through any of the people below:

  • Jeff Crowley or Cornelius Baker or Amy Slemmer, National Association of People with AIDS, 202/898-0414;

  • Paul DiDonato, San Francisco AIDS Foundation, 415/487-3096;

  • Susan M. Dooha, Gay Men's Health Crisis, 212/337-3342;

  • Ernest Hopkins, Cities Advocating for Emergency AIDS Relief, 202/429-8847;

  • Michael Kink, Housing Works, 212/966-1300;

  • Christine Lubinski or Allan Yount or Deborah Ashner, AIDS Action Council, 202/986-1300;

  • Miquelina Maldonado or Margaret Burton-Owens, National Minority AIDS Council, 202/483-6622;

  • David Lewis, Anne Donnelly, or Ryan Clary, Project Inform, 415/558-8669.



  
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This article was provided by AIDS Treatment News. It is a part of the publication AIDS Treatment News.
 

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