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Bruce Walker: [00:00:00] Thanks very much. Thanks, everybody for coming. Thanks to all the speakers and organizers, and everybody else and the Cold Spring Harbor. I'll start just by saying a few words about myself. I grew up in Boulder, Colorado. I went to the University of Colorado. That's where I was first exposed to research. I did a chemistry project. It was really esoteric gas chromatography. I came to the slow realization [00:00:30] that there were probably two people in the world who were interested in the outcome of the experiments I was doing, and I was not one of them.


I went off to medical school, and then to my internship at Mass General, really convinced that I was going to take care of patients. I was a back-row kind of a guy, and I really loved the clinical medicine. Thought I was in a place where everybody knew everything.

And then something really strange happened, similar to what Paul [Volberding] [00:01:00] described. A patient came in, young guy being treated for TB, mental status changes. Of course, it had to be that this guy had somehow developed TB meningitis. In fact, when we started working him up, he had lymphoma, Kaposi's sarcoma, pneumocystis carinii pneumonia, and a disseminated CMV infection. Nobody had ever seen anything like it. They said, "You'll never see something like this again." Then a couple of weeks later, another patient just like that showed up. [00:01:30] 

That really made me realize that, as physicians, we're on the front lines. We're going to see the first emergence of new diseases. Then something else really pivotal happened, and that is, this guy, Bob Gallo, came to Mass General in May of 1984, to talk about his discovery. To me, that was just really thrilling to think that they had taken patient samples, and actually, from those, had figured out [00:02:00] the viral etiology of HIV.

I went on to become an infectious disease fellow now thinking that research really did make a difference. I had another co-fellow with me, some of you might recognize, in my group that year, Michel Nussenzweig. At any rate, I was in an environment where really there's an emphasis on learning from patients. I looked for a mentor. I found Chip Schooley, who was working [00:02:30] with Marty Hirsch. They've taken on somebody else you might recognize there, David Ho, who was a year ahead of me working on antibodies.

Bruce D. Walker is director of the Ragon Institute of MGH, MIT and Harvard.

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Chip's idea was that I should work on T cells, in fact. He said cytotoxic T cells, and he said it's so fast. I didn't really even understand exactly what he had said. He helped dictate a grant application for me to submit as an NRSA (National Research Service Award). We submitted that, and the review [00:03:00] came back that basically said, "This is a terrible idea. HIV is an immunosuppressive illness. You're never going to find T cell responses to this, that's the whole problem." So Chip said, "No, no, this is a good project. Let's rewrite the grant and resubmit it." At this time, I was still a clinical fellow. I did some more reading on it. It actually, from the feline leukemia virus field, seemed that it made some sense. We resubmitted the grant. This time I understood what was in the grant. It came back actually with a [00:03:30] worse score than the first time. The review said basically, "You really didn't get it, did you? We said this was a terrible project."


At any rate, we had made a mimeograph copy of this and sent it to the American Cancer Society. Got funded, and so off I went to try and study T cell responses. The first thing I did was look for CD4 cell responses and it was complete bust. We found nothing in these AIDS patients we were studying from our clinic. I thought, "Maybe those reviewers [00:04:00] were right." Chip said, "No, no, let's look for CD8 T cells." In order to look for CD8 T cells—we had access to CD8 cells from infected patients. We didn't have a way to express HIV envelope on CD4 cells. Because of that, Chip sent me off to another laboratory.

There's a lot of swagger in this slide, I think.


I got sent to [00:04:30] Bill Haseltine's lab, over on the left there. Bill started me on a project to try and express envelope. I worked for nine months. There was one condition, and that was that I was not allowed to talk to Joe Sodroski, or Craig Rosen because they were doing really important work. I adhered to that. I worked for nine months. I got nothing in terms of usable data. Every time I tried to express envelope by a variety of different measures, it never worked.

One Saturday when I was completely despondent [00:05:00] Joe Sodroski came up and said, "What's wrong?" I thought, "He didn't tell me I couldn't respond if Joe asked me a question." I told Joe what was going on. Joe said, "Well, why are you doing that? We did that a year and a half ago. We know exactly why that won't work." I said, "What?" [chuckles] I went home, and I talked to my wife. I said, "I'm out of here." I talked to Bill on Monday, after that weekend, and Bill said, "Oh, [00:05:30] yes. Yes, I forgot. Let's have you work on this other project instead." I just thought, "Research is not for me, I've tried it twice." But my wife pulled me off the edge of the roof, and said, "You committed two years to this, just do it and see. Don't be deterred by minor little inconveniences like this."

I then, a week later, Joseph Sodroski came to me and said, "There's a paper [00:06:00] that just came out in Nature. You should go read that. It might be useful to you." It was this paper from Bob and Bernie [Moss] (b. 1937) about vaccinia virus constructs. (1) I read through the paper, and just became euphoric at the end of the paper when I read this sentence that said, "Recombinant vaccinia viruses should prove useful for making target cells," which was what I was supposed to be doing. Here was my ticket back to MGH, and out of my current circumstance. So I went back to MGH. [00:06:30] Marty Hirsch knew Bernie got in touch with him. We got the vaccinia constructs, and we started looking at them.

Much to our surprise, this slide actually was the first piece of usable data that I generated in my postdoctoral career, and I was now about 15 months into it. On the left are the target cells of a control lac target, and envelopes expressing target. These are B cells. On the right, in the box [00:07:00] at an effector to target ratio of 100 to 1, we were seeing specific killing of HIV envelope expressing cells. This was really exciting, but we thought, "Actually, we haven't done the controls yet." We had to establish some B cell lines on control patients from the laboratory, this took about six weeks. When we did the experiments though, what we found was that in the controls, there was no evidence at all of something going on. [00:07:30] We went on to do that in more patients.

Actually, to prove the reviewers wrong, we published this paper coincident with Fernando Plata and Brigitte Autran, with Patrice Debré, showing that, in fact, HIV specific CD8 T cells existed in infected individuals. (2, 3) The problem was nobody really believed it, because we were claiming that we could take blood directly out of people who are infected with this progressive illness [00:08:00] where we were getting CD8 cells to directly kill virus expressing cells at unprecedented levels of killing. The other problem was that we had not really nailed the HLA Class 1 restriction on this, and so there was a lot of criticisms about the paper. I realized my career was floating on this. I had been taken aside by a professor at Harvard before the paper was published, who said, "Do not publish [00:08:30] this paper. This will be the end of your career. This is definitely artifact."

So I had a little sweat under the brow. I realized that part of the problem, I thought, was that we were mixing up CD8 Class 1 restricted killing with some contaminating ADCC that we were seeing in these assays using envelope. Bernie had developed a reverse transcriptase expressing vector. [00:09:00] We got that RT expressing vector, and what we saw was terrific specific killing of autologous target cells. But now, when we looked at allogeneic target cells, as this example here, expressing just one shared HLA allele, we got no killing. It looked like it was restricted.

The problem was, all of the B cell lines I had matched five of the six different HLA alleles that this patient expressed, and [00:09:30] all of them were negative. That meant one thing; either what we were seeing was really weird, or the restricting allele was that one allele that I hadn't tested. Again, I had to go back. I had to find somebody that expressed that allele, I had to establish the B cell line, which took about six weeks. Then we did the experiment, and the experiment basically, was setting up all these different cell lines, took all day to do that, went into incubation at about four o'clock in the afternoon. [00:10:00] The incubation went for about six hours, and about ten or eleven o'clock at night, I was harvesting these things. I was in the small room where we have the gamma counter, and the results started coming off. I knew that I had to get this one cell line. If it was killed, then we were right, and this really was a Class 1 restricted CD8 T cell response. If it wasn't killed, I was basically screwed. [00:10:30] 

I'm watching these things come off, and the controls come off, and they're perfect. The other lines completely replicate in terms of showing nothing. Each time it takes a minute for the next group of data to come off. So I'm sitting there waiting for the next minute, and it's this one cell line. If it's going to be positive, then it's going to be great. The number flashes up, and it's wildly positive. I just felt this incredible sense of elation. And that very [00:11:00] second, a two by three-foot metal ceiling panel fell out of the ceiling, hit me. I ended up on the floor with a gash on the side of my face. [laughter] And—I've never really shared this story before. I told people locally. I told my mentor, but I haven't really disclosed this publicly. I don't know exactly what that means. [laughter] And I don't know exactly how it happened, but it's the absolute truth. At any [00:11:30] rate, we were able to move on then and show in fact, through another paper, that this was a real thing. (4) This was all stuff that we had done by studying patients who were HIV infected.

About that time, I got a phone call from Susan Buchbinder who said, "We have this cohort in California where we thought everybody was going to die who's HIV infected." She said, "We're 12 or so years out in this cohort, and some of these people are still entirely [00:12:00] well with normal CD4 counts." I thought, "Wow, that sounds really, really bizarre. I'd love to study those people." About the same time, I got referred a patient in Boston, and these are the notes that I was taking. He was telling me about, back in 1978, when he was in the seminary at Yale, right before Thanksgiving, he had these symptoms. They're hard to describe, but the sudden onset of weakness, it felt like he was frozen in the mud. Terrible headache, went to the hospital. He was hospitalized 7 to 10 days [00:12:30] and they never figured out what it was. He was a hemophiliac. In 1985, when the blood test became available, they tested him and figured out that this was when he had seroconverted. He came in, unlike every other patient who ends in the clinic that day, he actually looked healthy. Everybody else looked terrible with progressive HIV infection. His question was, "How long am I going to live?" I said, "They've made a mistake. You're probably not infected. We better test you again." We tested him, and in fact, he had [00:13:00] antibodies. To me, this was really a pivotal point where I thought, "Oh my God, there are some people that actually seem to be surviving this infection." Mark Feinberg was at the Whitehead [Institute] at the time and had just developed an assayed test for viral load. This guy, remarkably, had an undetectable viral load.

That really prompted us to dive into this quickly. Also, as we were doing this, we wrote another grant, I'll come to that in [00:13:30] a minute. The idea was, this guy must have CD8 T cells. We tested those. He had the strongest CD8 T cell responses we'd ever seen. If HIV followed the rules of biology, then this guy would have to have an HIV specific CD4 cell response. We dusted off those original assays I'd done when I'd first come into the lab. We tested it, and lo and behold, this guy had a phenomenal HIV specific CD4 T cell response. [00:14:00]

We found one other patient like this, and were convinced that these people that controlled spontaneously actually did have CD4 responses, that HIV could induce these. We wrote a grant, and the results from the grant came. The review came back, and they said, "You only have two of these patients, so we really don't know the relevance of this." We didn't get the grant. We, again, resubmitted it, and we ultimately got it. We were ultimately able to show that, in fact, not only was there an association of these cells with control, but also [00:14:30] if you treated people immediately in acute infection—and here, again, it goes back to the patients. We went down to the outpatient clinic, found people who were coming in with an acute viral syndrome, tested them by HIV RNA, found those that were in, that were acute HIV infections, immediately treated them, and saw how the generation of these really strong responses. (5) We moved on from there to test a hypothesis that, what if you could treat people early interrupt therapy, reboost their immune [00:15:00] responses, could you actually get them to control? In fact, we were able to show that, in a study published in 2000, that if you treat it early, and did these serial interruptions, you could actually boost people's immunity and get them to control. (6)

The problem was, it wasn't durable. In fact, in the followup study in 2004, once they broke through, they had much more rapid CD4 declines. (7) The virus was just winning out in these battles. We also were fortunate to collaborate with David Baltimore [00:15:30] and we're able to understand other reasons why this T cell response that should have been working, wasn't. (8) Nef was protecting cells from killing, by down-regulating HLA Class 1. We saw in other studies that Philip Goulder did, that immune escape was occurring. (9) In fact, if you had escaped mutations that were transmitted, it actually resulted in a worse outcome, in this case, in babies that were [00:16:00] infected. We found that even in individuals that were controlling spontaneously after early treatment, that they could become superinfected, and their T cell response had no effect on that. (10)

We went on to basically ask a more fundamental question: could we go back to something that was completely unbiased and try and understand what was associated with control and lack of control by doing a genome-wide association study? This was [00:16:30] something that involved about 200 collaborators across the US, and around the world. We finally, through that study, were able to show that it was a set of amino acids, [unintelligible 00:16:43] Class 1 peptide-binding groove, that were associated with control and lack of control. (11) This, again, suggested that the hit that we got, again, suggested CD8 T cells.

While we were doing this, we were also working in South Africa [00:17:00] where, I think if you look at this next slide, you'll see—this was a photograph I took when we were working in a clinic at a mission hospital. Each line is a different patient on each page. You can see how many of the patients that were seen that day, for the first time, actually had a HIV antibody positive test. It was just overwhelming, but at the same time, it seemed like, "Wow, here is an opportunity to really do something at [00:17:30] the heart of the epidemic. With our collaborator, Salim Karim, and Jerry Coovadia (b. 1940), we set up a small laboratory, hired some people there with our NIH grants, realized we couldn't move forward if we didn't figure out how to treat people, or the government wouldn't allow it.

We set up a treatment program at a mission hospital. It was really led by Kaye Ajao and Krista Dong. We now had things together to be able to do this. We started pre associating. How could we have more impact? There were a lot of people that wanted to get involved. [00:18:00] Salim had this vision of trying to really build a more integrated research effort there. We had the idea that we might be able to go to US donors and help. We hatched this idea of building a research Institute. In 2003, the Doris Duke Medical Research Institute was opened.

Now, really, there were facilities there to really support the research, and that led to a number of other studies. Again, all patient-based, where we had [00:18:30] large cohorts looking and showing that the breath of the Gag specific responses was associated with lower viral load. (12) The first studies to show that PD-1 was actually involved in regulating immune responses in humans, was all work done in Durban by a really talented postdoc, and then junior faculty person, Cheryl Day. (13) This theme of learning from patients is something that's really driven us along, and has [00:19:00] really, I think, been critical to the field. 

We're obviously not the only ones that have been doing things in this area. Going back quite a ways, it was clear that HLA is very important to viral control, and there are a whole number of different studies that have shown that. (11, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23) Their CTL (cytotoxic T lymphocyte) correlate with decline in initial viremia, that's something that Rick Koup and Seph Borrow initially showed. (24, 25) [00:19:30] Probably two of the more frequently referenced papers in the HIV field. A number of groups have contributed to understanding that it matters what is being targeted by the immune response. (12, 26, 27, 28, 29, 30, 31, 32, 33)

A number of other people have contributed, particularly Mike Betts and Mark Connors, to understanding these issues about polyfunctionality and lytic granule loading as being critical to CTL function. (34, 35, 36, 37)

And then PD-1 and other immunomodulatory [00:20:00] molecules, we know a lot about that and about the fact that HIV is prematurely turning off the immune response. (13, 38, 39, 40) Then finally, viral mutations and immune escape, are critical issues that are limiting our ability to do much with this. (41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51) And then also, studies showing that these cells really can be potent, at least in vitro, why aren't they doing a better job in vivo? (52, 53, 54, 55, 56, 57, 58, 59, 60) There are also studies that have shown, particularly [00:20:30] from Louis Picker, that there are unconventional CD8 T cell responses that can be generated, as he has shown with a CMV model, that provides really startling protection to about half of the monkeys that get that. (61) We have data in press now, showing that those responses also exist in humans, although they're very modest. (62)

Anyway, we've continued to work in KwaZulu-Natal (South Africa). We were fortunate to be able to convince Howard Hughes Medical Institute (HHMI) [00:21:00] that this was a place to invest, leading to this KwaZulu Natal Research Institute for TB and HIV. This has created, now, even better resources to be able to study patients at the heart of the epidemic. The heart of the epidemic is really still a pretty desperate place. These are data from Salim, showing about a 10% per year incidence of new infection among young women, ages 18 to 23. These are people living in poverty. Poverty plays a big [00:21:30] role in this. We saw these data, and generated similar data ourselves, and realized actually, there's an opportunity here to do something different and that is to look at a timing of HIV infection that we haven't really been able to look at, which is the time of the upswing in viremia; from the onset of viremia to peak viremia. We set up a program called Females Rising through Education, Support, and Health. This is both a pathway out of poverty and an HIV prevention program. We [00:22:00] enroll women in this that are 18 to 23 years old.

Have them come in twice weekly, for empowerment life skills, and job training, and HIV prevention classes. At the same time, we do a finger stick blood draw, looking for acute HIV infection. This study, funded by the Gates Foundation, has allowed us to really work out the dynamics of hyperacute infection and know where we've been able to get multiple measurements on the upswing of viremia. [00:22:30] It's allowed us, by doing T cell assays, to show that there's this massive CD8 T cell activation that is not by standard activation, but actually, is activation of HIV specific T cells that rapidly become dysfunctional. (63)

More recently, really, for the last two years, we've been able to treat people immediately, once they've become infected, and here's an example. We're dramatically limiting the amount of viremia. Here's a patient that had four days. The week before [00:23:00] on Friday, they have an undetectable viral load. They come in the next week on Tuesday, and they have a viral load of 440 copies. We get that result back the very next morning. We immediately treat them, and you can see here that by Day 7, there's no more viremia.

What we've seen with that, is this dramatic difference in terms of the T cells that are detectable by tetramer staining here, at peak viremia. Now, rather than the cells lacking CD127, which is a functional [00:23:30] marker on T cells, now the cells actually wildly express that. There's a fundamental difference by limiting antigen acutely. Related to this, is that, I think what we're doing, is we're seeing now for the first time, what a functional prime that doesn't deplete CD4 cells is actually capable of doing, so we're really excited about this. We think this is a model that, we, through our collaborator, the collaboratory that's run by [00:24:00] Dan [Barouch] and then involves Merlin Robb and Nelson Michael, and Jintanat [Ananworanich], that we are going to be able to take the patients from our cohort, and the Thai cohort, and African cohorts that Jintinat and Merlin have, and be able to do immunologic intervention studies, and really try and understand what's going on here. I'll just show one slide that I think is really tantalizing, and that is studies that Dan has done separately, that show, really, this incredibly robust induction [00:24:30] with a vaccine of T cell responses in monkeys that are immunized after being treated in hyperacute infection. We're really anxious to see that forward.

We think T cells actually are here to stay for a while, in terms of being likely important to cure strategies, whether it's because of reversal latency and ability to control those, or whether it's trying to [00:25:00] reengineer T cells so that they can actually traffic into follicles by expressing CXCR5, and be able to hit the sanctuary there, are questions that are yet to be determined. (64, 65) Whether you can shift the response to subdominant T cell responses, as suggested by Bob Siliciano, I think, is something still to be shown. It's also questionable, as to whether—since a T cell can recognize a single peptide MHC (major histocompatibility complex) molecule on an [00:25:30] infected cell, that's not enough to induce a T cell response, but it's enough for an infected cell to be killed. There may be enough leakage, actually, in latently infected cells for them to be recognized. It's just that we're not getting the cells to the right place. (60, 65, 66)

I'll make some conclusions. Learning from patients that's showing us how the T cell response usually fails, but sometimes succeeds. Persons with controlled HIV infection, suggests that a functional cure is possible. Limited antigen exposure and acute infection enhances T cell functionality. [00:26:00] HIV-specific CD4 and CD8 T cells are likely to be critical to a functional cure, and are likely, through T follicular helper cells, to be critical for antibody responses. I'll make one plea, and that is that, so much of what we know in the context of HIV infection, comes from supporting cohorts that are well-pedigreed. That's how we got viral load. That's how John Mellors figured that out from the MACS study (Multicenter AIDS Cohort Study, 1984–2019).

All of our work has been critically dependent on this, and most people do not want to fund [00:26:30] cohorts. I think what we need is a way for investigators, in the same way, you can write a way for an antibody that's specific to a particular epitope, you can write a way for a sample of cells that are from a person with specific disease characteristics so that you can study them.

Just quick acknowledgments. We have a tremendous group of collaborators, and I've listed them here. I won't go through them in detail, but we'll stop there and happy to take some questions. [00:27:00] Thanks.


Bob GalloPeriodically of the statements like I'll make have been made by other speakers, so it's not really a question. The other day, we commented or I commented about what Max Essex did pretty spectacularly in Botswana. I want to say I had an opportunity to visit the places that Bruce just showed pictures of, and just was fantastic. [00:27:30] He's done a fantastic job in South Africa.

Bruce: Let me put that on our collaborators there. It's Salim. It's Jerry Coovadia and all those people. It speaks to the partnership

Bob: I know. Salim is going to talk, though. Salim is going to talk with a video, but no false modesty. You did a great job over there.

Bruce: Thanks.

John MellorsBruce, antibodies to immune checkpoints have revolutionized cancer therapy in the last five years. [00:28:00] Are we missing the boat on HIV infection and chronic viral infections [crosstalk]?

Bruce: Well, those studies are being done. I think they've been done slowly. We need those data, and so I agree with you.

John: There's a barrier, in that the cancer field is dominating the development [00:28:30] of those antibodies, and they look at chronic viral infections as secondary.

Bruce: Yes, and not a lot of motivation by pharmaceutical companies to get into this morass, and questions about the developmental pathway as well. That's a huge issue for everything right now; from vaccine development, immunotherapy, to PrEP studies, is that we've got really good [00:29:00] ways to get rid of virus, or at least suppress virus. It makes it much more difficult.

Larry CoreyBruce, what do you think is the way that one could bring immunotherapy to someone who's chronically infected? The whole issue of not being able to use an immunotherapy approach with any vector [00:29:30] or even adaptive transfer of cells. We know a lot, but yet we're not changing things.

Bruce: I think there's an opportunity to do that. What we're trying to do is, we're trying to start out where we're most likely to get a signal that we can work from, and that's why we're focusing. [00:30:00] We don't for a minute think that this is scalable to find people with hyperacute infection, but we think it's a way for us to understand what a really good immune response is, and what's required to that to get generated. Then we'll hope to build off of that into chronic infection. If we can't do something infection then it's really a moot exercise.

Larry: You're saying that there's something in T cell helper, or some other aspect [00:30:30] that's permanently damaged within a week or 10 days that lasts forever and is unrecoverable?

Bruce: Yes. That's unrecoverable under natural circumstances, but potentially reversible through intervention. I think the data, going back to the MACS Study and the work that [Robert H.] Lyles did, showed that something happens in acute infection. What we've seen from this study is that the magnitude and rapidity [00:31:00] of generation of CD8 T cells in acute infection, is associated with lower viremia. The quicker you get them, and the higher the magnitude, the lower the viral load subsequently, but we need to be able to do this so that we can consistently get people to undetectable.

Even if you get people to undetectable, the question is, is that going to be enough? Is a functional cure [00:31:30] a viable strategy in this day and age? I think that remains to be determined. Thanks very much. Oh, Robin?

Robin WeissI'd just like to echo what Bob Gallo said. I'm on the board of directors of K-RITH, which two weeks ago, merged with the Africa centers, now the African Health Research Institute. Your mentorship to people like Thumbi and Dungu up at the top then [00:32:00] and your ability to collaborate and make linkages, has been a real catalyst. I think beyond your own science, I really admire what you've done in KwaZulu-Natal. Thank you.


Bruce: It's been a collaborative effort. [chuckles]


[00:32:24] [END OF AUDIO]


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Found 26 search result(s) for Walker.

Page: Session 2: The Pandemic Begins, Early Discoveries (HIV/AIDS Research: Its History & Future Meeting)
... Chairs: Michael Gottlieb (UCLA Medical Center) and Bruce Walker (Ragon Institute of MGH, MIT and Harvard
Mar 18, 2021
Page: Session 6: Immunology and Prevention (HIV/AIDS Research: Its History & Future Meeting)
... Burton — How Does HIV Evade the Antibody Response? 6.3 Bruce Walker — Role of T Cells in Controlling HIV Infection 6.4 Barton Haynes ...
Apr 27, 2021
Page: Females Rising through Education, Support, and Health (FRESH) (HIV/AIDS Research: Its History & Future Meeting)
... Program run through the Ragon Institute, see 6.3 Bruce Walker — Role of T Cells in Controlling HIV Infection
Feb 12, 2021
Page: Bush, George W. (b. 1946) (HIV/AIDS Research: Its History & Future Meeting)
... George Walker Bush, b. 1946, President of the United States from 2000 to 2008
Aug 31, 2020
Page: Bush, George H. W. (1924–2018) (HIV/AIDS Research: Its History & Future Meeting)
... George Herbert Walker Bush, 1924–2018, President of the United States  from 1989–1993, and Vice ...
Aug 31, 2020
Page: 2.0 Michael Gottlieb — Introduction to Session 2 (HIV/AIDS Research: Its History & Future Meeting)
... 00 My thanks to the organizers and my cochair for conceiving the idea for this meeting. Bruce Walker has allowed me three minutes to say something at the start of this as a chair. It's ...
Apr 27, 2021
Page: 6.7 Salim Abdool Karim — Stopping the Spread of HIV in Developing Countries (HIV/AIDS Research: Its History & Future Meeting)
... treatment. It was in a whole range of different areas. Then finally, working with colleagues in the US, Bruce Walker and Bill Jacobs, in particular, we secured funding from the Howard Hughes Medical ...
Apr 27, 2021
Page: 6.2 Dennis Burton — How Does HIV Evade the Antibody Response? (HIV/AIDS Research: Its History & Future Meeting)
... invited to be here, and thanks to Bob Gallo, John Coffin, Mila Pollock, and Bruce Walker for the invitation. I didn't have any personal slides. I'll just tell ...
Apr 27, 2021
Page: 8.1 John Mellors — MACS and Beyond: Epidemiology, Viremia and Pathogenesis (HIV/AIDS Research: Its History & Future Meeting)
... apoptotic resistance cells. Alan: One more question from Bruce. Bruce Walker: John, how accurate a picture do you think we're getting from ...
Apr 27, 2021
Page: 8.6 David Baltimore — Bringing it to an End (And Where Are We Going?) (HIV/AIDS Research: Its History & Future Meeting)
... T cell receptor to use? We combined our efforts with those of Bruce Walker, who has shown that there are T cell receptors in elite controllers that are very specific ...
Apr 27, 2021
Page: 2.2 James Curran — Deciphering the Epidemiology of AIDS (HIV/AIDS Research: Its History & Future Meeting)
... Jim Curran: Thanks, Mike Gottlieb, and Bruce Walker, and all the organizers. It's nice to be here with all of the passionate, committed veterans working ...
Apr 27, 2021
Page: 1.5 John Coffin — The Origin of Molecular Retrovirology (HIV/AIDS Research: Its History & Future Meeting)
... been really an enormous honor and pleasure to be able to interact with Bob Gallo and with Bruce Walker to put it together over the last year or so. I'm going to focus on one ...
Apr 27, 2021
Page: 3.2 Samuel Broder: The First Clinical Trials of Antiretroviral Drugs (HIV/AIDS Research: Its History & Future Meeting)
... had to be there. I'd like to present my personal reflections, I was asked by Bruce Walker and others to give my personal reflections on the 00:00:30 initial treatment ...
Apr 27, 2021
Page: 3.4 Raymond Schinazi — Discovery and Development of Novel NRTIs (HIV/AIDS Research: Its History & Future Meeting)
... It's great to have you. Thank you also to John Coffin and Bruce Walker because it was unintelligible 00:00:14. Ray: Yes, well, I said ...
Apr 27, 2021
Page: 2.5 Françoise Barré-Sinoussi — Discovery of HIV (HIV/AIDS Research: Its History & Future Meeting)
... cure and cancer. Thank you very much for your attention. applause Bruce Walker (moderator): Thanks very much. We'll take questions and comments. Mark Harrington ...
Apr 27, 2021
Page: 3.1 Marty St. Clair: Discovery of AZT as the First Anti-HIV Drug (HIV/AIDS Research: Its History & Future Meeting)
... all glad you studied retroviruses in college. laughter Questions? Bruce. Bruce Walker: Marty, was there any pushback at the company about developing HIV drugs, given 00 ...
Apr 27, 2021
Page: 9.1 Jon Cohen — Responding to AIDS: A Journalist's View (HIV/AIDS Research: Its History & Future Meeting)
... take the drugs for life, especially if you treat people early enough, Bruce Walker had studied him, I believe, Bruce, didn't you? It raised a new ...
Apr 27, 2021
Page: Session 10: What Have We Learned? (HIV/AIDS Research: Its History & Future Meeting)
... Archives, Cold Spring Harbor Laboratory Bob Gallo John Coffin Bruce Walker Warner: 00:00:00 —Is maybe to have each of the organizers, take a minute ...
Apr 27, 2021
Page: 2.4 Robert Gallo — Discoveries of Human Retrovirus, Their Linkage to Disease as Causative Agents & Preparation for the Future (HIV/AIDS Research: Its History & Future Meeting)
... one second to thank and say what a fantastic job the coorganizers did, Bruce Walker is standing right next to me, and John Coffin, who was a ball of fire and sometimes ...
Apr 27, 2021
Page: 2.6 Tony Fauci — 35 Years of HIV/AIDS: Science and Policy (HIV/AIDS Research: Its History & Future Meeting)
... colleagues on the outside, to continue to follow the science. (50) Thank you. applause Bruce Walker (Moderator): We're open to 00:26:30 comments and questions. Yes, Mark ...
Apr 27, 2021
Page: 5.3 Michael Malim — Discovery of APOBEC Restriction (HIV/AIDS Research: Its History & Future Meeting)
... all, thank you very much to John Coffin, Bob Gallo, and Bruce Walker for convening this meeting and inviting me. It's quite a humbling experience really to speak ...
Apr 27, 2021
Page: 6.5 Emilio Emini — Issues in HIV Vaccine Development: Will the Future be any Easier than the Past? (HIV/AIDS Research: Its History & Future Meeting)
... observation from Rick Koup (9) and then, of course, all the work that was done by Bruce Walker and others during this period. (10, 11, 12, 13, 14, 15, 16 ...
Apr 27, 2021
Page: 8.4 Robert Siliciano — The Challenge of the HIV Reservoir (HIV/AIDS Research: Its History & Future Meeting)
... response through rapid evolution, as shown by George Shaw, Dennis Burton, Bruce Walker, and many others. I think we didn't fully appreciate this paradox when ...
Apr 27, 2021
Page: Session 7: Prospects for an HIV Vaccine (HIV/AIDS Research: Its History & Future Meeting)
... panel and then we we'll open it up to the audience. Dan Barouch: So Bruce Walker, Bob, and Glenda  asked me to say a few words about our personal ...
Apr 27, 2021
Page: 6.4 Barton Haynes — Development of HIV Vaccine: Steps and Missteps (HIV/AIDS Research: Its History & Future Meeting)
... Burton — How Does HIV Evade the Antibody Response? 6.3 Bruce Walker — Role of T Cells in Controlling HIV Infection 6.5 Emilio Emini ...
Apr 27, 2021
Page: 6.6 Robert Redfield — The PEPFAR Program to Treat HIV in Africa (HIV/AIDS Research: Its History & Future Meeting)
... Martin — Making it Simpler: A Single Pill to Treat HIV 6.3 Bruce Walker — Role of T Cells in Controlling HIV Infection Afghanistan Africa ...
Apr 27, 2021

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