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Rodrigues: Our next question is something a little closer to home. We know that your annual laboratory meeting is now quite an event, attracting, as I understand it, researchers from around the world. I was wondering if you could tell us a little about the evolution of that meeting, how it got started and how it evolved into the form that it has now?
Gallo: Our annual laboratory meeting is a large event today, and it does have a history of multiple transitions. I cannot remember the exact day, or even the year, when it began. But, as our group was becoming a little larger than a small group, we felt that we needed to evaluate where we were, why we were, and what we were on an annual basis. We needed to evaluate what we would be doing in the next six months or year, maybe even more intensively than it would be done on the outside of NIH because we had this assurance of funding, especially whether we should make a change in direction, and especially which person applying to the laboratory should we try to take. So it started as a retreat. At first, we held it right here on the campus. Then we thought, “Gee, it would be a nice idea to hold it where the phone does not ring and where nobody could interrupt us.” We thought of holding it away from the laboratory. We started meeting in some of our collaborators' laboratories, or in a farm out near Frederick. We did not stay overnight. We would go back and forth to the farm. It started with only our laboratory attending. We would look broadly at everything we were interested in and decide where we would go. This was some time in the early and the mid-1970s.
Then we started to invite our collaborators, of whom there were a few. There became more collaborators, and then our collaborators' collaborators, and it grew. We started having the meeting at hotels out in Gaithersburg [Maryland] and elsewhere.
Then we took some years off, years that were more years of frustration, and we did not have the meeting for–I do not know–three or four years maybe. This was precipitated by a meeting in Blackwater State Park. We were told never to come back to that state park because people were up all night, [Dr. Marvin] Marv Reitz was playing his guitar and other people could not sleep. People were making a lot of noise. It was like we were let out of our NIH cage. So we did not go back to Blackwater State Park. We took a few years off. It was appropriate to do so. Then we restarted in hotels or motels out in Gaithersburg. By then the Europeans were involved because we had those collaborators.
The numbers really increased with the discovery of HTLV-I and HTLV-II because the field of human retrovirology was now born. People were coming to learn about these viruses, more of them from Europe, in fact, than proportionally we would have expected. But it was still a moderate size meeting. There was our senior staff–say 20 people–and maybe we would have 40 from outside, so we would be 60, 70, 80.
Then all of a sudden came the disease called AIDS and the numbers increased to around 100 or so. After 1984, they were doubling every year until Dr. [Samuel] Broder put a cap on the numbers and the maximum is now 700. But, to be truthful for Dr. Broder, we had 800 people this year. He was among them, I think, but I thank him for not noticing. And so, the problems are now fire problems and being able to control it.
We lost something in the largeness of the meeting. We lost the intensity of discussion. We lost the flavor of a more personal relationship with people, real friendship. Now it has become a mini-congress, or maybe not even a mini one. It is a different beast now.
But we have always have used this meeting to develop our interests; not just cover exactly what we are doing, but broaden out our interests. It is not just an AIDS meeting. It is perhaps 60 percent AIDS. But it also includes quite a bit of cancer and we often have outside lecturers, very good ones generally speaking, who are in a field that our laboratory wants to learn more about. As an example, this year we had [Dr.] Harry Ginsburg, a leader on adenovirus. We had [Dr.] Peter Hans Hochschneider from Munich, a leader in hepatitis virus, giving special lectures. We had [Dr.] George Klein, on Epstein-Barr virus, giving a special lecture. We had [Dr.] Beech from Cold Spring Harbor on matters related to the cell cycle. Just to give you an idea of the variety, [Dr.] Judah Volkman comes every year and talks about blood vessel biology. We have our troupers that come every year, like [Dr. Thomas] Tom Waldmann, Judah Volkman, [Dr.] Hilary Kaprowski, [Dr.] Michael Feldman from the Weitzman Institute, [Dr.] Izaac Witz from Tel Aviv, the [Gunnel and Peter] Biberfelds and [Dr. Hans] Wigzell from Stockholm, half a dozen people from France at least, and a few from Belgium. These people have come annually for a long, long time.
In other words, out of the 800 there is a solid core of 100 people that is always there. This is not 800 people; this is 800 scientists. It is not like a congress. You can say the International Congress on AIDS in Japan may have had 10,000 people, but they probably had 1,000 scientists. Our meeting is a good meeting, but it is now seven days long. That is a long time for people to be there.
Harden: Seven days?
Gallo: Yes. From 8 o'clock in the morning until 6:30 or 7:00 at night every day for seven days.
Rodrigues: Do proceedings come out of your laboratory meeting?
Gallo: We do not like proceedings. We do not like to demand manuscripts. What we have done in the last few years is to ask at least some of the people who have given special lectures to make short synopses of them and we have published the abstracts in the journal called AIDS Research and Human Retroviruses. This year it actually starts with a chapter by me–a few pages by me–which is on the same kind of question you asked me. It is called “Reflections” on the meeting and it gets at it from an historical perspective. It is not about the people from outside our laboratory who came, not the interesting tales, but simply about the question you asked, the formation of the meeting, how it happened and why. I tried to focus on people who were in this laboratory and left or who are in this laboratory now. I am not talking about outside people.
Harden: I think Dennis is going to follow up later about our interest in perhaps getting some of the pictures of the annual laboratory meeting. Could we get copies?
Gallo: You can have all of them. My office can tell you about that, and there are extra ones. I know Latta Nerukah, who is at the Journal of NCI now, she used to take care of all of this. The last two years she did not, and [Dr. Genoveffa] Veffa Franchini next door did.
Harden: Good. We will follow up. I would like to come back to science for a moment and note that much of your AIDS research has already been detailed, again. Aside from what you have documented already in your book, is there any of that work that you would like to expand on, that more needs to be said about?
Gallo: Sure. I think Kaposi's sarcoma, for example.
Harden: I would like to come back to Kaposi's sarcoma as a separate issue because you have continued to work on that.
Gallo: If you want to know what I think are the major contributions of the laboratory–the contributions that I consider fascinating. Are you talking about AIDS? Is it just AIDS?
Harden: Just AIDS.
Gallo: The contributions of this laboratory, counting the... I am going to leave out key people and what they think is their great contribution, and I will speak as me, but really this is the lot.
First, I would say the idea that AIDS is due to a retrovirus. Even if the idea was imperfect, it was the idea that worked.
I would say, second, the evidence that HIV is the cause of AIDS came first and chiefly from us.
Third, the blood test, with the mass production of the virus, came from our laboratory, that is, a blood test that worked and a blood test that was put into operation.
Fourth, the nature of the genes of HIV came from more than one laboratory. It came from [Dr. Simon] Wain-Hobson and his colleagues at the Pasteur Institute, but it also came from our laboratory, particularly [Dr.] Flossie Wong-Staal, [Dr. Marvin] Marv Reitz, and Dr. Lee Ratner here, in collaboration with [Dr. William] Haseltine and with others like [Dr. Takis] Papas. So, defining the genome of HIV came partly from my coworkers.
The discovery of the tat and rev genes came partly from here, rev probably completely and tat partly, principally by Dr. Wong-Staal, but other people in the laboratory contributed to that.
That is five. Let us not number them. The discovery of the variation of the virus, ironically–because some people like to use that demonstration to indicate where there was a contamination–but we are the ones who discovered it first and published first, second, and third on the variation of the virus.
We also discovered and published first the variation within an individual, in other words, the micro-variation, of the virus.
We were involved with others–[Dr. Dani] Bolognesi and Repligen–in the discovery of the V3 loop in the HIV envelope that you hear much about. Popovic and [Dr.] Sue Gartner discovered the macrophage tropism of the virus. [Dr.] George Shaw, [Dr. Beatrice] Hahn, myself, and Flossie [Wong-Staal] discovered the brain infection with the virus. We documented the first heterosexual transmission with [Dr. Robert] Bob Redfield. We discovered for the first time the virus in plasma, viremia, with [Dr. Zaki] Salahuddin and colleagues.
We did the bulk of the epidemiology in collaboration with a bunch of other people in the early period to document the presence in different countries. I do not mean the epidemiology–that is wrong–the serology, the antibody testing, in a variety of countries, let us say.
We discovered human herpes virus 6 [HHV-6] as a possible cofactor in AIDS. By the way, Dr. Montagnier believes HIV is the cause of AIDS. He just is looking at some, I think, fairly obscure cofactors as possibilities. We are too. I think HHV-6 may promote disease progression, but I do not think there is any specific cofactor necessary. So, if you mean cofactor as something essential, I do not think there is any. If you mean something to make the disease go faster or slower, that is true of all human disease, and I think we should work on documenting such factors in HIV. It is appropriate.
We developed the first animal models and culture systems for Kaposi's sarcoma and there is extensive data available today on the pathogenesis of Kaposi's sarcoma. There is also a stream of subset observations from that, some of which have led to therapy.
In collaboration with Hybridon in Massachusetts we developed the first antisense RNA. They produced it, but we were involved as, I think, reasonably equal collaborators, for this antisense RNA against HIV which is now in clinical trials.
A recent discovery, as you know, is of the hormone, the first anti-tumor effect, of chorionic gonadotropin working on Kaposi's sarcoma in our mouse model.
We developed the first evidence that Kaposi's sarcoma can be a true malignancy. It [the paper on this] is now off to Nature. Before it was known to be hyperplasia only–non-neoplastic. Do you want me to continue?
Harden: I want to come back and go into some of these in more detail. I think Dennis wants to go into a few other puzzles at this point and then we will come back to Kaposi's sarcoma and some other topics.
Rodrigues: In our reading, we come across certain questions that seem to recur over and over again. Probably one of the continuing questions that comes up is, if we know so much about the virus, why is it that we still do not understand...
Gallo: Dennis is giving me a “meatball.” He knows I have answered that before. He knows how I answered it too. Okay. I understand the question. You do not have to go further. If we know so much about AIDS, why are we not able to cure it, or “How come we can't treat it, Doc? Why can't you do better?" I will sort of tell you why.
I do think we know a lot about AIDS. I think it is much more than people have portrayed recently. I think there is a tremendous wealth of knowledge about the biology of this virus and also about the molecular biology, and even about how it works. But that does not mean that we know anywhere near enough yet. I would like to point out the obvious, that you could know everything about the virus and not be able to solve anything. You might say, “That doesn't seem right?" But I once gave as an example to Nature magazine that I could know all there is to know about the Himalayas, every hole, every cave, every rock, their history, their origin, their evolution, its future, but I would not be able to climb these mountains until somebody else developed a new technology for me, such as the helicopter. It does not mean that if we gain every bit of understanding of the pathogenesis of AIDS that we are going to get to a cure. However, it is obvious that the more we understand, the greater the probability that we can climb the Himalaya mountains. It increases the probability of that occurring.
It is a tremendously difficult problem. If you think of any virus that persists, how many can you get rid of? Virtually none. If you have a persistent virus, by definition, you cannot get rid of it. We do not have therapy that gets rid of many viruses. But the AIDS virus is a nastier one and can kill. It is nastier than many other viruses, so we need to develop a whole new area of research, and that is antiviral therapy. AIDS will be the juggernaut of that. The timing is right because we know much of the molecular biology of the replication cycle of many viruses. I think AIDS will take the lead and that there will be spin-offs to other areas of virology. That will happen as surely as we are sitting here. AIDS will also take one of the leads in vaccinology. It already has, even if we do not have a vaccine for AIDS. Virus variation is complicated. We do not know why, but you do not get a very good immune response that is long-lasting, the kind you would like to see. It is complicated because if some viruses integrate and there is not the immune response right away, which is what happens, will you be able to keep the virus suppressed? If you can maintain that immune response of the right kind, yes. Animal models are not very good. Which one predicts for the vaccine? We do not know. Which one predicts for each other? They do not. Each animal model is giving us different data. Oftentimes we get protection in a monkey against SIV or HIV-2 and there is no immune correlate. What do we get out of that?
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