AIDS TREATMENT NEWS: Some see a backlash against the "hit hard hit early" philosophy. Some physicians say that is right for some people, but that others, especially those who have an excellent prognosis anyway for several years maybe we should hold the fort with a regimen such as d4T plus ddI, and reserve protease inhibitors, non-nucleoside RT inhibitors, and other treatments where viral resistance can develop rapidly, until we have better drugs and combinations available. How do you answer?

Dr. Ho: Some people are looking at failures on combination therapies which include a protease inhibitor, as an indication that the concept of hit early hit hard is incorrect. My view is the opposite, given what we have seen over the past year. The failures on combination therapy have generally occurred when patients are more advanced in the disease process, and have taken prior antiretroviral therapy, usually as monotherapy or dual therapy. And one must consider the issue of compliance or adherence; poor adherence is akin to hitting inadequately hard.

Those are the principal reasons for failure on combination therapy. Our experience suggests that when treatment is successful, patients maintain control of HIV replication on combination therapy. Most of them were drug naive, or at least without extensive antiretroviral drug experience. The earlier you start, the greater the chance of sustaining the antiretroviral effect. So the practical experience does support the hit-hard-hit-early notion.

ATN: When you are the treating physician, who if anybody would you suggest should not start treatment at all?

Dr. Ho: There are certain patients who are HIV infected, but have either a normal or slightly depressed CD4 count, and a viral load which is spontaneously quite low. Their prognosis without treatment is quite good, based on those numbers, and there is no reason to rush into any form of therapy. One could comfortably monitor their viral load and CD4, and delay making any decision on starting treatment.

ATN: A big concern is that many people are not ready to start this complex regimen, and do not have the commitment they will need to see it through for year after year after year. The fear is that they will start something and not be ready to maintain it.

Dr. Ho: This is obviously a very important decision. If the commitment is not completely there, then I would agree. If a patient cannot face a very complicated regimen for several years at least, then starting therapy may in fact be bad. Without the commitment, adherence will likely be poor, leading to drug failure, and many drugs will be used up. That would not be in the patient's best interest.

ATN: What would you say about treatments like d4T plus ddI that are not recommended in the guidelines, but are picked to be drugs where resistance tends to develop slowly--as intermediate between no treatment, and the full hit hard hit early?

Dr. Ho: I think if the situation were not as desperate, if somebody is pretty well off and wants to take that sort of approach, of reserving stronger drugs for later use, I think an argument could be made in support of that strategy. However, with a drug combination such as the one you mentioned, it is fairly clear that you cannot adequately control the virus, there will be residual ongoing replication, and some variant forms will eventually emerge. So the antiviral effect is unlikely to be very durable. And even though ddI may not be the most crucial drug to have in your arsenal, you will still use it up. It takes away one card that we may want to play in the future. Overall, I cannot endorse such an approach.

ATN: At the recent ICAAC conference there were posters on the correlation of the nadir of indinavir blood levels [the trough or lowest concentration of indinavir (Crixivan(R)), for example, in the blood between doses--which usually occurs just before the next dose], with how durable the effect was. If the drug level became too low between doses, viral resistance and rebound would likely develop. So there has been an interest in the community--maybe less so in industry--in individualizing doses, by checking blood levels when a person starts on a drug, to make sure it is being absorbed, and that the nadir stays high enough to maintain an antiviral effect. What do you think of this approach? Does it make even theoretical sense? And if so, what about the practicalities of getting it introduced.

Dr. Ho: It makes a lot of theoretical sense. When we first tested protease inhibitors, we noticed that there are lots of individual variations in drug concentrations. In those days we were doing pharmacokinetics regularly. The same dose could achieve concentrations that vary considerably between patients, suggesting significant individual differences in drug absorption and metabolism.

We found quite a bit of individual variation in how these drugs are absorbed and metabolized. If those concentrations could be measured easily and dosing could be tailored on an individual basis, this would certainly make sense. But on a practical level, even for researchers, it is not easy or inexpensive to get these measurements made. In clinical practice, it would be even more difficult.

ATN: Some researchers have told us that companies have not been cooperative with them in developing these tests--for example, refusing to provide pure samples of the drug to calibrate their tests. Have you had any such experience?

Dr. Ho: I do not know much about that. Many of the companies do not even do these assays [for drug levels in blood] themselves; they contract out to certain commercial laboratories that measure these drug concentrations by specialized chemical techniques. I find that on a practical level, it is difficult to get these measures done.

ATN: This may be a bit blue sky, but one HIV drug now being developed, T-20, will have to be given by injection. So they are looking at the infusion pumps, the little programmable ones that look like a beeper; I'm told they are working well for diabetics, for giving insulin. It would seem that this should be investigated for other antiretrovirals, since it would get around problems of adherence, the number of pills, food or no food, acidity in the stomach, and individual absorption from the GI tract. Most importantly, continuous infusion might provide better control of blood level and HIV replication. What do you think of eventually looking to an infusion pump for delivering some of the antiretroviral combinations?

Dr. Ho: We had some experience using such pumps many years ago, back in the late 1980s, to administer soluble CD4. We know it is do-able, although it will not be easy. Also, in testing the early generation of the Abbott protease inhibitor, the compound referred to as 77003, a pump was tried for a short period, because the oral pharmacokinetics were not good.

During those periods, the sentiment was that parenteral [injection] administration was so infeasible that we should move to oral medications. Today we have mostly developed orally available drugs; we are faced with the adherence issue, and people are thinking of ways to improve adherence. If we have a drug that needs to be administered not daily but occasionally, I think such a strategy may be an important adjunct. But I find it difficult to think that we are going to be able to administer three or four different drugs by a device such as that; on a practical level it would be quite difficult.

Instead, to deal with the adherence or compliance issue, I think it is more important for companies to develop drugs that are easier to take--for example, to move from three to two to one time per day. Many pharmaceutical companies in the HIV field have taken that on as an important objective, because the easier the regimen, the higher the adherence, and the higher the success. And of course some of the non-adherence problems are related to toxicity--so companies need to make related compounds that have fewer adverse effects. I think that on a practical level, these approaches might work better. Certainly I would not be opposed to trying the pump, but I think that daily use of injectable drugs would be tough.

ATN: I hear that in diabetes, people have no trouble wearing the device permanently.

Dr. Ho: But that is just delivering one drug, insulin. With our patients, it's unlikely that any patient will get just one drug. And some drugs could not be administered in intravenous or subcutaneous forms. And if the different drugs need to go into different solutions, then you will be constantly reloading the device with different drugs. If it were a single drug, as in diabetes, it might work.

ATN: When there is virological failure with a triple combination, what can people do next? We hear many anecdotal reports of people whose treatment has "failed" virologically with some of the protease inhibitor combinations, in that viral load comes back up but usually not all the way to baseline; however their CD4 count seems to stay high, and they seem to be doing well clinically. What do we know about what's going on? And how should these people continue their treatment?

Dr. Ho: There are several scenarios. Take the patient who is previously antiretroviral naive, who gets treated with a triple combination, who has good suppression for a while, then after some period of time, say a year, the viremia reappears. In that case, you could have viremia that bounced back to the prior baseline--which means that the virus is resistant to two or three of the drugs. The thing to do there is to change to a new regimen. Since the patient is previously drug naive, the doctor still has several other options to work with.

There is another scenario, however--closer to the one you presented. Viremia reappears, but at a much lower level. Therefore, that lower level does not seem to impact the CD4 count or the clinical picture. What do you do?

This is a difficult issue. Clinically and immunologically, you are still benefiting the patient by continuing the medications--because the viremia is suppressed compared to the baseline, and the CD4 count is still at a higher level. The concern here is that there is now residual virus replication; we are all aware of the possibility that resistant viruses will eventually emerge, and the question is, will that take a few more months, or will that take another year or two?

We do not know what the right answer is. For those inclined to be more aggressive, they may go ahead and add a drug, and see if they could get it back down to undetectable levels--to arrest the evolution of viral sequences, and therefore block the further development of resistant virus. Others do not like to add just a single drug; they would rather change the whole regimen. We do not have enough experience to know how persistent such a situation could be.

Then there are patients who have taken several drugs before, and begin a more powerful combination and suppress viremia for a period of time, but then the viremia comes back at some intermediate level. Here it is hard to make pronouncements or general guidelines about what to do; you have to deal with it case by case, depending on the specifics of the situation, the prior drug experience, and what options are left to come up with a combination of drugs that a patient has not seen before.

ATN: What could be said about the odds or percentages--either for naive patients starting a hit-hard-hit-early regimen, or people who have had much prior experience and have been through most of the drugs besides protease inhibitors, and then start their first protease-inhibitor-containing regimen? Are there any situations where we have fairly good data to let people know what their chances may be? And to what extent are the problems due to lack of adherence, and therefore under control to some extent by the patient?

Dr. Ho: We have some indications, but not much cohort or trial data to guide us. In drug naive patients who start these combinations reasonably early, and adhere to the combinations, in our experience clearly over 80% to 90% have durable suppression for over a year, and some have been on treatment successfully now for over two years. But adherence to these difficult regimens is a very real problem. And often it is hard to predict in advance who will stick to the regimen, and who will not. In addition to the true drug failure, we are going to have somewhere around a third who will be significantly non-adherent to the regimen--even in motivated patients such as our trial subjects.

But if someone is very confident that they can stick to a twice-daily regimen for several years, and if that patient is drug naive and reasonably early in disease progression, the chances of prolonged suppression are quite good.

On the other extreme are patients who are in and out of the hospital, who have taken several of the reverse transcriptase inhibitors in the past, and then start on a typical triple combination. I think the recent San Francisco General data suggests that about half of those patients will fail. That takes into consideration everything: the prior drug experience, the more advanced disease status, and includes any adherence problems.

ATN: Yet so far I have heard that most of those patients are doing well, even the ones who have virologically failed.

Dr. Ho: That is a very important point--what do you mean by failure? That failure in the San Francisco study was defined as any virus being detectable; it was a virological definition. If you have ongoing, detectable virus, the concern is that the result will be more resistant virus, more viral load, and clinical failure. But having a little bit of viremia but still having the virus under reasonable control is clinically very beneficial.

The San Francisco study was portrayed in the lay press as terrible news. It is certainly not great news, but not so bad if you consider the clinical perspective.

And you need to realize that was a chart review study, looking back at the early experience with these treatments, in a hospital setting with advanced patients. That study design was prone to yield a more pessimistic view of combination therapy including a protease inhibitor.

ATN: I talked to Dr. Deeks, and we published a short article on that report ["ICAAC: Newspaper Headlines Misleading on Protease Inhibitor Failure," AIDS TREATMENT NEWS #281, October 17, 1997], to give people a different perspective than was misreported in the headlines.

ATN: Now there is data suggesting that a viral load below 400 copies may not be good enough; for the most durable viral control, you would really like to know that you are below a much lower cutoff, for example below 20 copies. The practical problem is that most patients cannot get the Ultrasensitive test that goes down to 20. As a stopgap, would it make sense to use the available test and look for a result of zero, no virus detected at all, instead of a number which is above zero but below the quantification limit of 400?

Dr. Ho: If the threshold of detection is 400, then there is no point in reporting a specific number below that 400; that would confuse people, and is not reliable.

You can find some patients who consistently have a result between 20 and the lower limit of the more available viral load tests [400 or 500]. Some people on the modern combination therapies are in that category.

How we interpret this situation, and whether we should do anything about it, is a gray area now. It is unlikely that a viral load of, say, 150 copies per ml will be associated with rapid progression and clinical disease. So clinically, you probably do not need to do very much to modify whatever the patient is on. However, this test result tells us that there is continuing viral replication; the virus will continue to evolve, and we have to be careful about a breakthrough later on. Since there is not a lot of clinical experience to guide us, some people are saying we should just follow these people carefully; others, if there is flexibility, would add a drug to see if the virus could be dropped below 20 copies per ml. But these assays [those which accurately measure viral load when it is below 400 copies] are only available today to research groups, or to patients who pursue it directly with the companies.

ATN: On viral resistance testing, what role do you see for these tests--both now, and in the future, for selecting which drugs to start somebody on, or which drugs to change to?

Dr. Ho: I think these tests probably could be very helpful, if they could be made simpler, with faster turnaround, and at some reasonable cost, say equivalent to a viral load test, or only slightly above that. We do not have anything today that meets these criteria; however, a number of people and companies are working toward those goals.

These assays will most likely be useful when a patient goes on combination and is failing it, and you need to need to know what to do next. While the patient is still taking the failing regimen, so that the viruses are breaking through despite the presence of the drugs, you could take the virus and measure their resistance profile, and get a reasonable reflection of what is going on. Then if the viruses are, say, resistant to two of the drugs the patient is taking, and sensitive to the third, you would use that drug in combination with two or three other new drugs. In that setting, resistance testing will be fairly useful.

One has to be careful about using any of these tests on a patient who has gone off the drugs already. Say the patient has taken AZT plus 3TC in the past, and has resistant virus to those two drugs, but the drugs are no longer being used. The resistant virus would revert back to a minority population, say only accounting for 5% of the viruses. The resistance assays used today are not sensitive enough to pick that up; you would miss it, and get a false sense of security, and may use drugs that would be doomed to fail.

So while the patient is on the medication, I think the tests are useful. But once the patient has gone off the drugs, and the resistant virus is the minor population, the tests we have now would not be reliable. There are ways to deal with this; surely the companies will come up with such strategies in the future, but they are not there yet.

Therefore, at the start of therapy, I think that taking a history [of previous antiretroviral drug use, where some of those drugs are likely to have been discontinued] may be at least as useful as measuring the virus--unless you are dealing with a patient who was infected with a drug-resistant virus in the beginning.

ATN: Looking ahead maybe three to five years in the future, do you think most of the usefulness will be from the phenotypic tests [which see how well the virus can grow in the presence of drugs] or the genotypic tests [which look for mutations associated with resistance to particular drugs]?

Dr. Ho: I think that ultimately we would like to have a phenotypic assay--the same approach used successfully for testing antibiotic resistance very quickly in the laboratory, to strep and staph and other pathogens. The genotypes are quite difficult to interpret; because of mutational interactions, their clinical consequences are often very difficult to predict. We want a phenotypic assay in the long run.

Dr. Ho: Here is one project I would like to see pharmaceutical companies take on. They know how to make protease inhibitors now. They could take a very resistant virus--for example, a virus highly resistant to indinavir--and crystallize that protease, and start the whole effort over, and develop a second generation protease inhibitor that will attack the drug-resistant variants. Companies have been through the process [of developing protease inhibitors], they know the strategy, and these strategies have been quite successful over the last few years. Why not repeat it, and come up with compounds that would be active against the viruses that are resisting the first generation protease inhibitors? I think that would add a lot to the arsenal for our patients.

ATN: Isn't this the approach that Abbott used to develop its second generation?

Dr. Ho: I am not sure if that is the strategy they used. ABT-378 has greater potency against the wild-type virus, and good pharmacokinetics. It tries to overcome the resistant virus through greater potency and higher drug concentration. To my knowledge, it was not designed against a resistant virus.

I think this process might work better if we start from scratch, with a drug-resistant viral protease.

ATN: What do you see, in the next several years, on eradication possibilities?

Dr. Ho: We are learning quite a bit. Eradication is still a goal; it is not something we or anyone else has achieved so far. But we are learning a lot about different viral compartments, and how quickly they could be eliminated once strong therapies are applied.

The available therapies have helped us eliminate over 99% of the virus in infected individuals. But we are learning about additional viral compartments. In our patients who have been treated very early and very hard, and have received this treatment two years now, we are still finding a residual pool of virus resting in certain CD4 cells, in a very quiescent way. This poses a new obstacle to deal with.

Some people would say it means eradication is not possible. But those of us who are working on the science look at it differently, and say this is information we need to achieve eradication. Now with this information, how do we move on? How do we flush that residual pool out, how do we protect the individual from that virus reactivating and spreading the infection?

Much fairly exciting basic research is underway, by several groups. If we go back a few years to 1994 or 1995, we would not have predicted that we would be dealing with such a small pool of virus after a year and a half or two years. But on the other hand, the cells that contain this virus are quiescent, so they will not turn themselves over very fast. So we need to think about continuing antiviral therapy, but also using certain immunological strategies to activate those cells so they could be flushed out. It poses a new obstacle; but it is a scientific challenge which has certain theoretical solutions. The research groups engaged in these issues are taking that on. It is quite exciting from a scientific perspective.

ATN: Is there much re-infection with a different strain of HIV, after one strain has become established?

Dr. Ho: We can show in monkeys that re-infection occurs; we do know from the various recombinant viruses that we find in people throughout the world, that dual infection or superinfection must occur on occasion. But on a practical level, within our patients, there have been precious few documented cases of superinfection. Some groups have looked for evidence that this has occurred, and have not found it.

ATN: Over the next three to five years, what are some of the particular drugs and treatment strategies and approaches that you think we should be keeping an eye on?

Dr. Ho: Some of my answers will be the standard ones you hear from others. We will have several more reverse transcriptase inhibitors, both nucleoside and non-nucleoside. We should have a few more protease inhibitors. But I also think that the companies that are making these drugs will come up with equivalent ones that are less toxic and easier to take. If we could move some of the protease inhibitors from three times a day to one time a day, it would be a major advance. Some of the companies are working toward these goals.

Also, a couple major pharmaceutical companies are working on integrase inhibitors, a potentially very important class of drugs.

The recent breakthroughs in chemokine receptors, as cofactors necessary for viral entry, have led to much screening to find drugs that might inhibit one or several of these co-receptors. At the screening stage, the effort has been quite successful; there are many "hits" [compounds that work in the laboratory screening tests], and they are being pursued. We probably will not hear much about them for another year or two, when they get to toxicity testing, and some to clinical studies. But there is much activity already.

And there are other new kinds of drugs being developed, such as T-20 that attacks the envelope fusion process, and other drugs that attack the viral protein.

ATN: What do you see as the most important issues to leave with our readers?

Dr. Ho: The issue of eradication, the goal, what we are learning about the obstacles, and the strategies to deal with those. The failures: it is important that patients understand what are the principal causes of failure; many of them involve treating advanced-stage patients who have prior antiretroviral therapy. And the issue of adherence.

When we hear statistics, we have to understand under what setting were the numbers generated--and not just walk away and say that study says it's 90% successful, and this study says it's 50%, so somebody is wrong. One has to interpret all of these results in the context of the patient population that is being studied.

Also, the word "failure" is being thrown around without a precise definition. Is it virologic failure, is it clinical failure? We need to keep this difference in mind.

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By Linda Grinberg

On October 13 several treatment activists met with Glaxo Wellcome representatives in Research Triangle, North Carolina, to begin discussions on the design of expanded access programs in 1998 for the experimental nucleoside 1592 (abacavir) and Glaxo's new protease inhibitor, 141W94. Community representatives proposed a new framework for a widened expanded access program promised for early next year. Both community and company representatives agreed that the present model for expanded access seems outdated, and based on the needs of an earlier time in the AIDS epidemic. The goal of the proposed new model is to restructure the entry criteria to enable people to make treatment decisions that are consistent with the current guidelines.

The underlying principle for expanded access programs should be to provide the drug to patients who are otherwise unable to construct a *viable treatment regimen based on the current treatment guidelines*. Community representatives felt it unnecessary to further restrict entry criteria using viral load, CD4 counts, or specific drug failures, unless required by the FDA. Such restrictions, which micromanage medical decisions, have often denied access to people who were in the best position to benefit from the new drug. The proposed simplified entry criteria would be supported by educational materials provided to patients and their physicians to help them make wise and proper choices, rather than seek a drug just because it is "new."

Glaxo representatives did not voice any objections to the proposed framework for an expanded access program for 1592, although they were uncertain whether the FDA would support it. In addition, they said that any widened program would also be influenced by the recommendations of their physician advisory panels. Community representatives acknowledged the need to call for new thinking on the part of the FDA regarding the role of expanded access and will use best efforts to persuade FDA to accept this definition or principle of expanded access.

It was agreed by both company and community representatives that, since no one could accurately determine the actual need or demand for the drug, no arbitrary limits be set on the total number of patients served by the program, and Glaxo will make every effort to make all available drug supply not used to support the clinical trials available to patients. Historically, most expanded access programs have operated this way, without pre-established numeric limits. Number-limited programs became commonplace after the introduction of protease inhibitors, due to supply problems. These programs have been extremely unpopular and often unfair. Programs with an open-ended commitment have been far more satisfying to the community, even when supply shortages temporarily slowed recruitment.

Community representatives suggested that the same principle--to support patients who are otherwise unable to construct a viable treatment regimen based on the current treatment guidelines --also be used as the basis for expanded access to 141, at the earliest possible date. Glaxo Wellcome felt that information on cross resistance was vital to the design of an expanded access program for 141, since it would provide much needed guidance about where and how to use the drug. Preliminary data will be available in early 1998, as well as additional safety data, and therefore Glaxo felt we should revisit the issue in February.

Community representatives felt very positive about the simplified approach to expanded access, and hope it can serve as a model for future programs. This new concept will put the power of making specific medical decisions about treatment back in the hands of the patient and his or her own physician. Current programs, in contrast, seem to leave that power in the hands of the companies, the FDA, and others who would attempt to write arbitrary and rigid entry requirements.

(Linda Grinberg is the founder of FAIR, Foundation for AIDS and Immune Research, in Los Angeles, and a board member of Project Inform.)

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On October 17 Glaxo Wellcome announced that it was broadening the entry criteria for its experimental antiretroviral 1592 for persons with AIDS dementia complex (ADC). "To qualify for enrollment, patients must be 14 years of age or older, have evidence of HIV-associated dementia as defined by the American Academy of Neurology and/or an MSK (Memorial Sloan Kettering) score of 2-4, and have either experienced deterioration of ADC status despite treatment with Retrovir(R) (zidovudine; AZT) or are not taking Retrovir due to intolerance." The major difference is that now patients can qualify with moderate or severe dementia, while previously severe dementia was required.

At this time about 500 patients have received 1592 in clinical trials, and an additional 400 are receiving it through expanded access programs.

To be considered for enrollment, patients should have their physician call Glaxo at 800-501-4672, Monday through Friday 8:30 a.m. to 5:30 p.m. Eastern time.

A two-hour video on Qigong (pronounced "chee gong," traditional Chinese therapeutic exercise) will be aired in four half-hour installments on a number of cable channels in Los Angeles and Orange County. The showing began November 4 on Channel 50; check listings for dates and times in your area.

The videotape is also available for purchase, to benefit the Immune Enhancement Project in San Francisco; for information call 800-835-6555.

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In AIDS TREATMENT NEWS #281, the "Linezolid, New Antibiotic..." article misstated the location of the 37th ICAAC meeting, September 28 - October 1. The meeting was held in Toronto.

The error occurred during last-minute editing, and was not the mistake of the author.

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By John S. James

The major AIDS service organizations today started over 15 years ago as small, community-based activist groups--often created independently of older philanthropic and service organizations, which usually failed to address the epidemic because of public attitudes around AIDS. The need to build from scratch in response to a deadly emergency led to the creation of many thousands of separate AIDS organizations. Meanwhile, a few of the largest ones have become multimillion dollar agencies; and conflicts have arisen as they have tried to consolidate service delivery (either to increase efficiency, or to dominate the field, depending on one's point of view). In addition, some clients believe the larger organizations have become a remote, bureaucratic, self-serving "AIDS Inc.," setting their own priorities and agendas without meaningful public input or accountability.

What is new in San Francisco is that some of the discontent is now coalescing publicly; many persons who have been unhappy about how AIDS services are prioritized, organized, and delivered are now learning about each other, when they did not know each other before. The San Francisco AIDS Foundation, as the largest service agency in the city, has been a primary target, but far from the only one.

AIDS TREATMENT NEWS focuses mainly on treatment, and we are not close enough to the service agencies to form our own judgments of their programs. But for better or worse, this developing controversy is likely to affect the future of the AIDS community. Many of our readers may be interested, so we are listing some sources for more information.

On October 28, a public meeting called the Accountability Forum was sponsored by three well-known San Francisco organizations: ACT UP/Golden Gate (415-252-9200), the San Francisco Log Cabin Republican Club (415-522-2944), and the Harvey Milk Lesbian/Gay/Bisexual Democratic Club (Chris Romero, chair of the HIV Committee, 415-751-5364). Speaker after speaker related nightmarish experiences, and little was said in defense of the major AIDS agencies. For more information, contact the sponsoring organizations.

A new group, the Accountability Project, has started a Web site, http://www.accountabilityproject.com. Besides press releases and other background material, this site includes controversial transcripts of client focus groups run for the San Francisco AIDS Foundation, with the names of speakers removed to protect their confidentiality. The transcripts, not intended for publication, were obtained by independent activist Michael Petrelis.

The Accountability Project also has a toll-free telephone number (888-583-3411) for people to call and tell their stories, good or bad, about experiences with AIDS services and organizations.

Defenders of the San Francisco AIDS Foundation have called for maintaining respectful discussion and debate. They note that there is not enough money to provide all necessary services--and that critics have often contradicted each other when demanding how services should be changed or prioritized (even when speaking in the name of the same organization). They point out that board members and senior staff of the Foundation have been willing to meet repeatedly with the critics, to explain what the organization is doing and why. They note that priorities of the Foundation are set by the board, which includes many people with HIV, some of whom are also clients of the Foundation--and that members of the public, with advance notice, can usually attend part of the board meetings (other parts of the quarterly meetings are often held in executive session), and can usually address the board. (They also note, however, that in many cases it may be more productive to talk with board members outside of the board meetings, which must focus on routine business -- or to meet with the senior staff responsible for the programs or policies at issue.)

A major dispute has concerned openness of board meetings of the San Francisco AIDS Foundation. The current policy is:

"If members of the public wish to attend a meeting of the board of directors, written notification must be received by the board chair at least 48 hours prior to the meeting. The request should contain the following information: name of individual who wishes to attend the meeting; purpose in attending the meeting; contact phone number where Board Chair can reach requester. The Board Chair will contact the individual at least 24 hours prior to the meeting to confirm receipt of the request and when appropriate, offer an invitation to attend the board meeting." Another procedure has been published for those who wish to address the board.

For more information about attending meetings, addressing the board, or bringing concerns to the San Francisco AIDS Foundation in other ways, call Joe Fera, San Francisco AIDS Foundation, 415-487-3053. For general information about the Foundation, see its extensive web site at http://www.sfaf.org.

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