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Harden: Would you talk some more about the workshop itself? Who do you remember being there? What else do you remember? What were the major points in your talk?
Curran: I do not remember exactly. I am sure I presented whatever data we had under surveillance, some fairly crude makeshift slides, with the latest numbers that we had, because we were conducting active surveillance of the problems in the United States. I described the cases as a single new public health problem. And it was intentional that we called our task force, as awkward as it sounds, Kaposi's Sarcoma and Opportunistic Infections, because we wanted people to understand that this was one problem. We were committed to that concept; and we would present our data by the number of cases of Kaposi's sarcoma, the number of cases of opportunistic infections, and the number of cases of both. In every case, they paralleled each other. They were all going up; they were all in the same age groups; they were all in the same places. So this was really one epidemic.
I would have presented some preliminary information and said that our next step was to find the cause and intervene. Once the cause had been identified, we could demonstrate how to intervene. What we like to do, of course, is stop the problem. So we were into trying to find out if there was something easy to do. In order to do that, we wanted to talk to as many living patients as we could. We devised a questionnaire, 30 pages or something, and flew out to talk to every living patient that we could find.
Harden: Do you have a copy of that questionnaire somewhere?
Curran: Harold Jaffe might.
Harden: We would like to have a copy of that original questionnaire.
Curran: We flew all around the country, and when we were finished, we could say that the average age of patients was 35, so they were not very young men. Also all of the patients were gay men, and they were living in areas of high opportunity for gay men. They were living in strong gay communities: San Francisco, New York, and Los Angeles. The other thing was that the men were all openly gay. That was one of the things that struck me. There were no closeted gay men. My previous experience with sexually transmitted diseases in the gay population was different from that. Here was a spectrum not only of homosexuality, but, even more important, of openness. Most of these people were living in openly gay communities, in an openly gay lifestyle. They seemed to have large numbers of partners, and they were getting a rare condition. There were also other things associated. They all went to the same clubs. Most of them used poppers or isobutyl nitrite or amyl nitrite, and they may have been exposed to other things in their environment.
But, from the very beginning, since we came from an STD background and had been studying hepatitis B, this really looked like a hepatitis B viral pattern. Our top hypothesis was always that an infection was causing this. But that was not going to be an easy one to combat. I mean, we wanted to make sure that we were not missing an easy solution. Had it been something like isobutyl nitrite, for example, it would not have taken us very long to get rid of that as a risk. That would have been a much more pleasant outcome than a persistent lifelong transmissible virus.
Harden: By the time of the symposium that the Cancer Institute sponsored in September 1981, had you seen any cases in women or children or any other groups?
Curran: The cases of drug users were not well documented in terms of risk. It was December 1981 when the articles in the New England Journal of Medicine, by Masur and Siegel and Gottlieb, came out. Masur's patients were all minority men. They were reported drug users, but they were all deceased by the time of the report. People were saying, “Maybe these are really gay men that are selling themselves to get drugs or maybe they had similar drug exposures.” That did not seem too plausible, but Siegel, from the same city, had cases in gay men, so maybe they were. It was hard to demonstrate that it was occurring in other groups initially.
Harden: So it was after that September symposium that you were moving out with your questionnaire and getting more information.
Curran: Yes. We began a case-control study in October. In that study, we restricted cases to gay men. The controls were matched for sexual orientation and city of residence at the time of the onset of illness; and they came from STD clinics or private physicians' offices.
you in charge of this study?
Curran: I was in charge of the New York City group, and Jaffe was in charge of the California group. We had maybe one or two cases in Atlanta. We interviewed 50 cases, and 203 controls. Then we used the standardized questionnaire and the standardized specimens, and the papers from those results were eventually published in Annals of Internal Medicine in about 1983. We started the study in October of 1981. We interviewed about 90 percent of the living cases in the country.
Curran: We did another study–it was a cluster analysis–that began in 1982, and started with some gay men with AIDS who reported to [Dr.] David Auerbach in Los Angeles. Do you know whom I am talking about?
Curran: They reported that there was a gay fundraiser in the late 1970s, which a man and his lover attended. The lover and three or four others at the table at the fundraiser–there were maybe about 1,000 people at the party–all subsequently died of AIDS. Dr. Auerbach contacted Bill Darrow, who interviewed all the living cases in the L.A. mega-metro area, of which there were nine. Nine of the first 13 cases, whether living or dead, were linked to each other through sexual contact. Eventually they linked up to 90 other people around the country through sexual contact, which was 40 percent of the first 220 gay men reported with AIDS in the United States. By doing personal interviews around the country in 1982, Dr. Darrow and colleagues were able to link together the network of sexual contacts.
The next important link was the cases in hemophiliacs. Dr. Bruce Evatt, the head of CDC's hematology group, announced at a task force meeting: “There is an old man with hemophilia from Florida who had Pneumocystis and who died.” The man died of Pneumocystis. I said, “What?” We were all thinking blood–it was going to be in the blood supply if it were caused by a virus like hepatitis B. But not everybody wanted to believe this. There were a lot of other hypotheses. So we said, “We really have to watch out for this and investigate carefully.”
Bruce was also the medical director of the Hemophilia Association of Georgia. Sure enough, a couple of weeks later, we had the report of a case of PCP in a person with hemophilia from Colorado. We sent [Dr.] Dale Lawrence (currently an NIH scientist) to investigate.
Dale was an extremely compulsive physician and scientist. He went out and spent two weeks with this man and his family. He reviewed everything he could possibly ever know about his personal and medical history, and obtained specimens. He recorded every lot number of concentrate the man had ever received and concluded that the man was heterosexual with no history of injecting drug use. At the time, there were no other cases in Colorado. It remained possible that he had an underlying tumor responsible for his immunosuppression.
This man was the second hemophiliac to die of Pneumocystis. So we went to Bill Foege, the Director of CDC, and said, “We've got these two cases. It is getting real suspicious but we could only investigate the second one.” We all agreed that if it happened twice, it was going to happen three times, and there would have to be two living cases before we reported a pattern. Then the third case was reported in a young boy from Ohio, and he had never been out of the state. So Dale Lawrence went up there and spent two weeks investigating this case.
In the summer of 1982, at a symposium at Mt. Sinai Hospital [in New York ], Dr. Irving Selikoff invited [Dr.] David Rall, the director of NIEHS at the time, to discuss AIDS. Dr. Rall, true to the institute's perspective, suggested that the cause of AIDS was somehow related to environmental exposure. Others touted their own special hypotheses. The Director of the CDC, Bill Foege, was going to talk about the infectious disease hypothesis.
Foege went first, and he announced, “In this week's MMWR, there will be an article describing three AIDS patients with hemophilia, and we think this makes it look very much like it is a virus that is transmitted in the blood, in concentrates, because hepatitis is transmitted in these.” All of the other speakers changed their etiologic hypotheses to co-factors on the spot.
One of the things that I was doing for the meeting, in addition to assisting in drafting Foege's talk, was trying to get people together for the next meeting and trying to make sure that the gay community and the blood bankers and others were all on the same page, so that we did not end up with a lot of cacophony. We did not want the gay community coming out and denying this or volunteering to donate blood or anything like that. So I was trying to get leaders in the gay community, nationally and in New York, to have representatives come to the AIDS meeting–it was not called AIDS then, but it would soon be called AIDS–where they could meet with the scientific community and the blood bankers to make a concerted effort to deal with the problem.
Hannaway: The Hemophilia Foundation people and so on.
Harden: This must have taken a lot of diplomatic skills, given everybody's particular interests.
Harden: Do you want to talk more about that?
Curran: I think that probably the most historically important activities that the CDC did were things up to the March 1983 prevention recommendations. I mean that I think the period from June of 1981 to March of 1983 was when the CDC made its most difficult, but also most productive and important contributions.
I am particularly proud that we were able to investigate and determine the emerging epidemiologic patterns as quickly as we did and develop consensus in the scientific community and amongst the public. The CDC set an international example for surveillance, for moving the envelope forward, and for getting everybody on the same page. The scientists really started to believe that this was a virus when the hemophiliac cases became known, and they started to be interested in searching for a virus at that point.
Hannaway: So it was the CDC's skills in epidemiology and...
Curran: Yes, but also in convincing and communicating to people and getting people together, especially scientists, blood bankers, and the gay community. These were a lot of unnatural partners. It was not just cancer and infectious disease. AIDS for a time was identified with the gay community, which did not have a lot of reason to trust many people in government, especially as this was still a relatively small problem in the larger picture. There were a total of 1,000 cases by early 1983. That is not a lot when you think about it. There were still 15 or 20 states that did not have any cases yet.
Harden: The problems in the gay community have been fairly well documented and talked about in a lot of the literature. On the question of the safety of the blood supply, there has been a lot of criticism of the blood bankers. But we have talked with people like [Dr.] Harvey Klein–who heads the NIH Blood Bank–about what happens when blood bankers inform the public that the blood supply may be in danger. Dr. Klein said that the blood bankers did not want to be irresponsible and panic people unnecessarily. You, on the other hand, were sitting here believing, after seeing the data on the hemophiliac cases, that there possibly was a virus in the blood supply. How do you decide at what point it is worth panicking people if necessary to safeguard the blood supply?
Curran: The answer to how fast to do it is somewhere between how fast we do it now and how fast we did it then. In the pre-AIDS era, we accepted enormously high rates of hepatitis in the blood supply. For hemophiliacs, it was universal that they would get hepatitis. The concentrates themselves were not heat-treated or inactivated, and the products were pooled from thousands of donors. It was just expected that the benefits of getting these concentrates, which were saving a lot of lives, were greater than the risk of hepatitis. So we were in an era when the blood risk paradigm was not as important as the benefit paradigm. And a concern that what are a few more new infections when, after all, we have hundreds of thousands of cases of hepatitis. I mean, the blood bankers had a different historical perspective. If up to 5 percent of the people who got transfusions get hepatitis, in those millions of transfusions, what were two or three cases of Pneumocystis, especially when the technology for prevention did not yet exist.
The other part of it was that the people who were from blood banks were pathologists, and, in fact, clinical pathologists for the most part. They were not infectious-disease people. They did not receive funding from or communicate closely with the CDC. They received more funding from the NIH, and even then, the funding came not from NIAID or NCI, it was from NHLBI [National Heart, Lung, and Blood Institute], whose concern was not focused on infectious diseases.
Bruce Evatt and, occasionally, I would go to blood-banking meetings. We would give our presentation, and then we would leave. Then the blood bankers would talk to each other about how the suggestion that the blood supply might be infected could not possibly be true. They would bring in NHLBI people, and they would talk to them, and, of course, they did not believe it either. Some said, “We have seen this forever, this Pneumocystis stuff.” So that was just the way it was. That was their historical perspective. Now, were they wrong? Yes, they were wrong, in retrospect. Of course, they were wrong. Is it understandable? Yes, sure. They are portrayed, ten years later, as being self-protective, evil people who were killing their patients, but I think that is overstated.
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