Office of NIH History
In Their Own Words: NIH Researchers Recall the Early Years of AIDS
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Harden: I appreciate that.

Quinn: Does that answer that question?

Harden: Yes, it does.

Quinn: What I would like to do now is bring the discussion back to AIDS, what was happening with AIDS during all this, because this is...

Hannaway: Right on the same wavelength.

Harden: We are on the same track.

Quinn: When I came here for the interview–remember I told you Bartlett wanted to know, what is this guy like? You know how it is to go through the interview process.

They presented a case which I will never forget, nor will he. It was at ID [infectious diseases] rounds and it happened to be a woman. This was very interesting. It was a woman who had Pneumocystis carinii pneumonia, which was being described at the time in a few gay men. But this was the first time it had been seen in a woman.

Harden: This is August, September, October?

Quinn: This is April of 1981. I was interviewing; I was not here yet. I flew in.

Harden: This was before the first publication?

Quinn: This was before the publication, but word was out that there were a few of these cases. Although that was not discussed too much at the conference. Both John and I remember this very well, because they presented this woman with this pneumonia, and we started saying, “Well, she is probably....” They showed a photograph of her. She was very thin and malnourished, and we started talking about Pneumocystis outbreaks in post-World War II orphanages in Europe. That is where Pneumocystis was first really epidemic in people. It had always been described in bone marrow transplant patients and those having heavy cancer treatment, but the woman did not have a cancer and was not undergoing chemotherapy. But she had Pneumocystis. So we said, “It must be the malnutrition, and she is like these infants [in the orphanages].” We could not explain it any other way. But when the first report from the CDC came out-–which was what, May? Was it May?

Harden: June.

Quinn: It was June. The two of us clicked and said, “Could that woman have the same disease as those men?” We quickly went looking through the hospital records: Were there any other cases? There were no other cases of Pneumocystis in people that we could not explain. That was June of 1981. So that was, “All right, who knows what she had,” because she subsequently had died in the interim, and she was lost to follow-up. Nothing was left.

Then once more and more was known about this disease, the two of us kept coming back to this case, because we were sure that that woman, who was a prostitute here in Baltimore, probably had gotten AIDS sexually transmitted by someone or it was injecting-drug use. She had come down with it quite suddenly and she did not have the long incubation period that some do. She probably had been recently infected but was a very aggressive, rapid progressor.

But then the CDC report came out. Up to that point, I had not ever suspected that the men that I was working on in Seattle had any major immunodeficiency, nothing like what was being described in New York. I had not seen any of these skin tumors called Kaposi’s. I had not seen major pneumonias. The people that I took care of had intestinal infections, and that was all they had. But once I read the reports, I became interested. But I could not study it any more in Seattle, where my big cohort was. I had to move to Baltimore. So I started studying it here right away, and I became, I guess you would say, the first clinician at Hopkins to take care of patients with, I think we started calling it GRID then, gay-related immunodeficiency disease. I started building up a small clinic population of people with this disease and studying them. My first impression, with all the sexual transmission activity that was going on, with these intestinal parasites and other infections, was that it was an overwhelming infection. There was so much infection, it was overwhelming and immunosuppressing the people. I did not think it was a separate, new virus. We are talking about 1981. I thought that their immune systems were overwhelmed by these intestinal infections. That is what I had been studying for two years, so it seemed logical. And I was invited to the first task force meeting on AIDS–that conference that was held at the NIH, not down in Atlanta–which was just being formed.

Harden: The NCI Conference in September 1981?

Quinn: Was that when it was? No. I may not have been there. It was one that I will never forget, because it was at the NIH and [Dr. James] Jim Curran was there. It was to focus on what the infectious etiology might be.

Harden: So this was after everybody had decided that it was infectious. That was later, then.

Quinn: Yes, that was later. So, it was not the NCI one. I was not involved in that.

Harden: I had to peg it now, but there was a report from the New York Health Department in June of 1982 about hemophiliacs and women and babies, and it suggested blood transmission.

Quinn: Right.

Harden: This is the point from which I date the thinking about infection, but it may not be.

Quinn: Infection. Well, I had been thinking infection, but infection from the intestine that was then wiping out the immune system. My whole training was infectious diseases. So I figured this was an infection that was hitting the immune system. But I was not a virologist, so I did not even really think of pure virus. I just thought this immune deficiency was a secondary effect from the intestinal infections.

I started doing work on that, started studying the patients immunologically, looking at their cell immune response, taking out their T cells and working with that. When flow cytometry came, I quickly went to Ken Sell and said, “I need an instrument; I need to study this,” and I have the instrument up here. It has been updated since, obviously. I started studying the patients’ flow cytometry, their CD4 cells and how they went down, and their CD8s.

Harden: Now, this was after that conference. Would you talk about that conference and its impact on your thinking?

Quinn: The conference that I attended, at which Jim Curran was present–I do not know if he chaired it or co-chaired it–but he was up at the platform the whole time, always criticizing, always cajoling, always getting us to think. Interestingly, it was not a big meeting. It was a small meeting. Of course, the numbers of infections had not gotten very high; the number of cases had not gotten very high. But a lot of interest in the community was being generated, and so we went down to the NIH. I gave a presentation saying that this disease could be a result of these intestinal infections, and that was about the time my paper was getting accepted for the New England Journal. There seemed to be a lot of interest in that, that this was a secondary effect. Other people were saying it as well as me.

Then individuals–I remember [Dr. Robert] Bob Yarchoan from here got up and said it could be an enterovirus that was doing this. Also, he and I had been looking at blood specimens by EM [electron microscopy], and we saw little viruses in there that we thought were parvoviruses. In fact, they probably were, in retrospect. But we said, “Look at this virus. This is in their blood in a couple of patients, not in people who do not have this disease.” So we started looking at the parvovirus.

And I remember Jim Curran. That was my first meeting with Jim. He would get up and say, “All right, come on. Tell me more about this.” He would say, “You do not have the right control group, you do not have this, you have to get more patients, you have got to do this.” So he was saying, “Here are your negative effects, here are the positive effects, and let us move from there.” He did that with just about every presenter that spoke. I respected him right from the very beginning. I thought, “This guy’s really quite active.” Then he and I got to talking, found out we went to Notre Dame together, and we became friends. I just wanted to get it clear that he and I developed a fairly good working relationship and it has always remained that way.

Harden: He has promised me that we can interview him.

Quinn: Oh, yes. I am sure he will.

Harden: He is the only CDC person that we may have the authority to interview.

Hannaway: Yes, unfortunately.

Quinn: Is that right? In any event, I was working away trying to learn something about the weakness of the immune system, first of all, trying to classify it immunologically, because not many people had done that up to that point. And [Dr. Clifford] Cliff Lane, who was working in our same institute, was working on the B cells. His early paper was that there was a B-cell defect. I was working on macrophages and the reticuloendothelial system and why these people got opportunistic infections. That is where I was doing these clearance studies–they are in the early publications that you will see–and we found that there was a complement defect in these patients.

What we were all trying to do then was to describe the breadth of the immunologic deficiency. I was not really looking for a cause at that point. I did not have that expertise. And although we dabbled in it with those EMs, I was sort of limited at that. I was developing clinical skills on how to recognize the disease and how to care for the patients and treat their opportunistic infections. So every case that was seen in those early days here at Hopkins was referred to me immediately.

Hannaway: Did you have any more female patients?

Quinn: No. The female was a red herring. It was the first case of the disease that I ever saw, and that is why I brought it up. It impressed me that it was a woman and not a man, because everyone else was talking about men. For the first six months of this, I barely heard a word that any women were getting infected.

But that was all soon to change, because the Haitians were starting to be recognized as a risk group. This was the next phase in my AIDS career: the Haitians getting identified as a risk group and generating a big controversy. I will stop at that point, yes, before we get to Haiti.

Hannaway: We had noticed that you had obviously become knowledgeable about this syndrome early on, and that by 1983, you were presenting a paper at the Infectious Diseases Society meeting, which was held in Wilmington, Delaware. Then the next year the paper was published in the Delaware Medical Journal. You were already an authority...

Quinn: Right.

Hannaway:...on AIDS by that time.

Quinn: With reference to the Delaware issue, I started to get recognized in the region because I was the only one taking care of these patients, and it was because of my familiarity with working with them in Seattle. All of a sudden, I became known as a person who knew how to investigate their diseases and their infections and how best to diagnose and treat them. They were comfortable coming to me because I had a good reputation of working with such infections in Seattle. I was called upon a lot at that point to give talks on what this clinical entity was, so that was probably why I was invited up there.

Harden: Now what I want to do is to shift for a moment, before we continue the chronology, and ask you a question that we have asked many people, just to get your reaction. At this point, let us take it where we are in 1981-82. If AIDS had struck in 1955 instead of when it did, how would the medical community have responded to it? Would they have recognized it? Would they have been able to make any kind of response, and if so, what?

Quinn: I think the spread of this disease among a select segment of the population immediately draws a certain amount of attention that something is going on. These are homosexual men. Why is this happening? Would it have spread as rapidly in 1955 as 1979? I do not think so. A lot of things socially were changing in the 1970s that were much more hidden in the 1950s. Homosexuality existed, obviously, but not the magnitude of gay bathhouses and promiscuity that was sanctioned, supported, and encouraged in that community in the mid-1970s. That is what made that disease spread like wildfire.

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