Scientists Mark 25 Years of HIV Research In May 1983, the first scientific papers were published describing the possible connection between a retrovirus and the development of AIDS. The virus went on to become known as HIV. Experts discuss whether, 25 years later, scientists any closer to a cure for AIDS or to a vaccine to prevent HIV transmission.
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Scientists Mark 25 Years of HIV Research

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Scientists Mark 25 Years of HIV Research

Scientists Mark 25 Years of HIV Research

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You're listening to Talk of the Nation: Science Friday. I'm Ira Flatow, and as I say, for the rest of the hour, we're going to get you up to speed on the latest AIDS - HIV news. It has been - it's hard to believe, it's been 25 years since French scientists announced the discovery of HIV, the virus that causes AIDS. And since then, it has been a daunting nut to crack, this virus. Researchers have tried to get a basic understanding of how it operates so they can figure out how to stop it.

Treatment, of course, from the very beginning was a high priority, while the search for a vaccine came later. And that's been a very frustrating and unsuccessful search so far. The recent failure of two clinical trials suggests that a vaccine is not around the corner. So in the meantime, doctors have struggled to manage a disease that has reached epidemic proportions especially in the developing world.

But thanks to treatments that keep the virus in check, HIV/AIDS can be managed as a chronic disease, at least for those of us who have access, and can afford the life-saving medications. And some prevention strategies are working. Others are not. Which ones are they? We'll talk about all of this stuff for the rest of the hour.

If you'd like to get in on our conversation, our number is 1-800-989-8255, 1-800-989-TALK, and in Second Life, you can join us in Science Friday. Look for our Science Friday Island there, and step up to the group of folks sitting in the chairs, and sit down and you can ask your questions.

Dr. JOHN MOORE (Microbiology and Immunology, Weill Medical College, Cornell University): Thanks for having me, Ira. It's a pleasure to be with you again.

FLATOW: John Moore is professor of microbiology and immunology at the Weill Medical College of Cornell University here in New York. Welcome back to the program, Dr. Moore.

Dr. MOORE: Thanks for having me, Ira. It's a pleasure to be with you again.

FLATOW: You're welcome. Sarah Schlesinger is an associate professor of clinical investigation at Rockefeller University and the Aaron Diamond AIDS Research Center in New York. She joins us today from Raleigh, North Carolina. Good to see you again, Dr. Schlesinger.

Dr. SARAH SCHLESINGER (Clinical Investigation, Aaron Diamond AIDS Research Center, Rockefeller University): Ira, it's a pleasure to be here. Thank you for having me. And hi to - hi, John.

Dr. MOORE: Hi, Sarah.

FLATOW: I'm surprised you know each other.

(Soundbite of laughter)

Dr. MOORE: We've been in the research community for a long time.

Dr. SCHLESINGER: We're old friends.

FLATOW: I'm sure. Let's talk about this disappointing setback for the AIDS vaccine in recent months, the failure, in one clinical trial run by Merck, another one in South Africa. Dr. Schlesinger, what's happened here?

Dr. SCHLESINGER: Well, I think that the trial to which you refer is really one trial that failed, or didn't get the result that we hoped. And another trial that was stopped before it really began. So the trial to which you refer was a phase three, or an efficacy trial, of what was regarded by many people in our field as the most promising vaccine candidate, and a candidate is any vaccine that is not licensed.

And that was a vaccine to prevent HIV infection that was based on an adenovirus, a different virus, a common virus that causes colds, that was genetically engineered to contain three genes from HIV. And this was a promising candidate. It's been tested in small animals and nonhuman primates, and had gone through extensive evaluation in small trials in people as well, and it had been moved forward in an efficacy, or field trial, which is the only way to know the vaccine actually works.

So an efficacy trial is a trial where you go into an area where many people are getting infected. You evaluate that rate of infection. You then, of course, for ethical reasons, bring in all of what's necessary to reduce that infection with the methods we know, education, clean needles, condoms, et cetera. And then you come back with your vaccine and with informed consent, you ask people to - who you know to be at risk either to receive the vaccine or to receive what's called a placebo, or an inert, in this case, it was just salt water.

And then you follow those people. And you see who gets infected, usually over two years, sometimes a little bit longer, and if all of your infections - because you know that - from your research that these people are likely to get infected, occur in those who received the placebo, then the vaccine worked. And it they recur - or if they occur equally in the two groups, then you know your vaccine didn't work. And unfortunately, in this trial, not only did the vaccine not serve to protect the people who we had hoped that it might protect, there was a small group of people who had preexisting immunity to the adenovirus, the vector, if you will, for the vaccine, that seemed - more than seemed, that were made more susceptible to HIV infection by receiving the vaccine. So this was - the vaccine trial itself, I think, was not a failure. Because like any experiment, you don't know the answer 'til you start it. And it got an answer. It was not the answer we wanted.

FLATOW: Well, that's the question I have. It's sort of like why try - why go into a trial if you don't think you know something about how it's going to work?

Dr. SCHLESINGER: Well, I mean, that's the 64,000-dollar question. And of course, one never does an experiment to which one knows the answer...


Dr. SCHLESINGER: Whether it's an experiment in the laboratory or whether it's a human clinical trial. If we knew the answer, we wouldn't have to do the work. And that's the conundrum. One of the great challenges of developing HIV vaccines is we really don't know what works until we move forward to human clinical testing. There are many kinds of information that we can gain before we get there.

For instance, you know, how it performs in small animals - and one of the limitations is, unlike, say, with a tetanus shot, where we have what's called a correlative protection. So if I give you a tetanus shot, I know that two weeks later, I can draw your blood and I can measure what are called neutralizing antibodies, something about which John is extremely expert. And I know that if the titer, I think it's over one to 260, you're protected. And if it's not that, you're not.

So if I have a new tetanus shot, I can get a small number of people together. I can give the old tetanus shot to some. Of course, with informed consent, I can give the new tetanus shot to others. I can draw their blood. I can go into the laboratory, measure this antibody and say, ah, this is better. I have a higher titer. It's lasting longer. It's more durable. You know, a variety of different things. That's called a correlative protection.

We know what to measure in the blood that correlates with protection from disease. So nobody's ever been exposed to tetanus. I haven't had to go into a group of people who are at risk for tetanus, because tetanus is a very low-risk disease, obviously. So because we know the correlate, we can move forward with great ease. There is no correlative protection that we know - we don't know what the correlate of protection is for an HIV vaccine.

Nobody has ever been protected from the vaccine. We're trying to learn what the correlate is through a variety of different avenues of research. One of them is by looking at people who are naturally infected with HIV and control the virus. These people are called elite controllers. Another group of - there are animals, nonhuman primates, who have been quite well-protected by what is called a "live attenuated vaccine." That's a virus that's killed a little bit, or disabled. And that seems to confer pretty good protection on nonhuman primates. But it's not safe. And so therefore, we can't move it into people.

So from those two groups of people and nonhuman primates, we can gather some information, but we don't really know what a correlate is. And this is one of the great challenges. The other problem that we have, one of the other problems, is we don't have a good animal model. So we have nonhuman primates that get viruses that are like HIV, but none get AIDS from HIV. So we don't have like, say, you would for anthrax. With anthrax, guinea pigs get a disease from anthrax that is almost identical to humans.

So therefore, guinea pigs are the animal correlate for developing an anthrax vaccine. You can give them the vaccine, you give them anthrax. If they're protected, terrific. If they're not, you know you have to go back to the drawing board. We don't have that for HIV. So these two great challenges really are - hamper our ability to move forward as we might with other vaccines...

FLATOW: Doctor, let me ask Dr. Moore a question. Why don't, Doctor Moore why don't we know enough about HIV to make these things happen?

Dr. MOORE: But we don't know enough yet to design vaccines that (unintelligible - audio problem). So that's what we were really looking for, or the field is really looking for, a reduction in the amount of replication or in severity of infection in people who became infected on the trial. So that was the primary endpoint, really. And there was no such effect.

Now, that then makes us all question why. Because it's important to find out why it didn't work. And as Sarah mentioned, the really unexpected result that blindsided everyone was the enhancement of infection in a subset of individuals. So more infections took place than were anticipated compared to placebo. And that really did take everyone by surprise. And this caused a major exercise in navel-scratching, head scratching over the past six months.

It's been very tough to try to work this out, and there's still a lot of ongoing studies that will hopefully point to the reason for this very unexpected result. And it's important that we find out, because the next planned trial is broadly similar trial conducted by the NIH of a similar but not identical adenovirus vector with an addition of a DNA boost, and there's now major debates going on about whether that should take place, whether and if so, in what format.

Because there's no point in reinforcing failure unless we're pretty sure that we're going to be able to do better. And those decisions are not yet taken. They're being actively discussed. There are committee meetings coming up later this month, because that's an important decision for the next several years of the field. Do we, do we try another virus factor, or do we hold our horses for a couple of years, and try and come up with something better? It's an important decision.

FLATOW: So there's some key that's still missing here, that we just haven't figured it out...

Dr. MOORE: Well, yes...

Dr. SCHLESINGER: There are several keys that are still missing.

FLATOW: Several!


Dr. MOORE: I mean, we don't know how to induce neutralizing antibodies at a level and breadth that is sufficient. And realistically, the only way to prevent infection with the vaccine, to truly prevent an individual getting infected, is with a neutralizing, antibody-based vaccine. That's not to say that a T-cell vaccine isn't useful, but it's not likely to prevent infection and we don't know how to do this.

I mean, we're learning more and more about the reasons why we don't know how to do it, and it's certainly not an impossible task. It's just an extraordinarily difficult one from a scientific perspective. The virus has learned to resist the action of neutralizing antibodies. It has to survive in a human organism that raises antibody responses against it, and it's evolved sophisticated (unintelligible) to ward off those antibodies...

FLATOW: So, does that mean we need to know just more basic research before we do this clinical trial?

Dr. MOORE: Sure.

Dr. SCHLESINGER: Absolutely.

Dr. MOORE: We need structures for one thing. You know, there's a lot of efforts going on to crystallize, or generate sophisticated electron-micrographs of the envelope glycoproteins in their most native form. And it would really help to know, to see, what we're trying to make. We're trying to engineer better versions of the envelope glycoproteins that are on the virus to act as superior immunogens. That's a major...

FLATOW: Was that a marker? The marker is on the virus?

Dr. MOORE: The parts of the virus that cause the virus to get into the cell is (unintelligible)...

Dr. SCHLESINGER: And which are also the parts of the virus to which the body makes an immune response.

FLATOW: I got you. Let me just jump in here for an ID. This is Talk of the Nation Science Friday from NPR News. Talking with Sarah Schlesinger and John Moore. Do you want to continue on that? That's an interesting point, the part that - what, Sarah, you were saying?

Dr. SCHLESINGER: The very part of the virus that binds to the cell, which allows it to infect the cell, and frankly, cause disease, is the same molecule that the body has to make an immune response to in order to fight it. So it serves both as a receptor and as an antigen. An antigen is anything that stimulates the immune system to make an immune response.

FLATOW: So, it should - in theory, the body should be able to recognize and glom right on to it.

Dr. SCHLESINGER: Well, one would hope so, but the great success of this virus is that the body makes a vigorous immune response. I mean, in the beginning of the epidemic, you know, 25 years ago, people thought that the virus was able to evade immunity. That's not at all what occurs. There's a vigorous immune response. It's just not effective. It's not - the virus is able to evade the antibodies that are generated.

And one of the points that John made, which I think is terribly important, is we have many vaccines against viruses that work very well. You know, the Jenner vaccine developed against smallpox in 1796, before anybody understood anything about cells, viruses, or the circulation of the blood, protected, you know, helped to eradicate smallpox.

You know, measles-mumps-rubella, all of those vaccines induced immunity. They induced both antibody and cellular immunity. So John was referring to this as a vaccine that was designed to induce T-cell immunity. That's indeed the case, but it's my understanding, John, and please correct me if you have a different understanding, the vaccines that work induce robust immunity in both sides of the immune system.

Dr. MOORE: Absolutely...

Dr. SCHLESINGER: And that's really, you know, it - this vaccine and other candidates are able to induce some degree of T-cell response, but what we measure, you know, are tiny little blips if you compare them to what you get from a really good robust vaccine, say, like the yellow fever vaccine.

FLATOW: 1-800-989-8225. A quick question before the break. Alex in Dearborn, Michigan. Hi, Alex.

ALEX (Caller): Hello, Ira. I have a question about - there was a program about phages, which is basically viruses that kill viruses. Is there any kind of research to see if there's a virus out there that kills AIDS viruses?

FLATOW: John Moore?

Dr. MOORE: This wouldn't work for HIV. Those phages work against bacteria. Essentially bacteria phages kill bacteria. They don't kill other viruses, and this wouldn't be an approach that would work for HIV. HIV is inert until it gets into the cells it infects. So you'd be asking for phages to kill the infected cells. I don't think that's a viable strategy.

FLATOW: But you're still coming up, trying to come up with your own strategy?

Dr. MOORE: Well, it's not that we don't know what to do. We know what to do. We just don't know yet how to do it. I mean, as Sarah said, ideally a vaccine should induce both T-cell immunity and antibody immunity (unintelligible)...

FLATOW: Could you describe the difference between those two, please? Describe...

Dr. MOORE: Well, you'd have to design the immunogen in different ways, because the two arms of the immune system stimulate it by different types of antigens. So it's difficult to make one type of vaccine that simultaneously does everything you want, and it may be better to go in and work with two half vaccines, as it were, and combine them, but so far, we're not succeeding in either arm...

Dr. SCHLESINGER: No, but...

Dr. MOORE: And we don't have a good T-cell vaccine that's good enough as the Merck results (unintelligible), and we certainly don't have an antibody (unintelligible) vaccine that's yet good enough.

Dr. SCHLESINGER: But John, when one induces - so, Ira, you asked about the two arms of the immune system. One makes a vigorous immune response. One makes antibody, which is a protein that circulates in the blood, but is a clear protein itself. And one also stimulates various different cells which will kill by direct contact.

So the antibody that's made is often referred to as the "humeral arm" of the immune system, which actually goes back to the Hippocratic for humerus, believe it or not, and cell-mediated immunity refers to the cells that actually define the infected cells that John mentioned. So when the caller asked about a phage lysing the bacteria, the infected cells, the HIV infected cells, are lysed by direct contact with what are called CDA or killer T-cells.

FLATOW: All right, stay with us. We're going to come back and take more questions and calls about the 25th anniversary of the discovery of HIV virus. Stay with us. We'll be right back after this break.

(Soundbite of music)

FLATOW: I'm Ira Flatow. This is Talk of the Nation's Science Friday from NPR News.

(Soundbite of music)

FLATOW: My guests are Sarah Schlesinger, associate professor of clinical investigation at Rockefeller University and the Aaron Diamond AIDS Research Center in New York, and John Moore, professor of microbiology and immunology at the Weill Medical College of Cornell University here in New York. Our number, 1-800-989-8225. Let's go to James in Hyannis, Massachusetts. Hi, James.

JAMES (Caller): Hello.

FLATOW: Hi there.

JAMES: Hello, doctors. I'm calling - I was infected in 1981. I've lived my entire adult life with HIV, and what you were saying about the CDA cells was very interesting to me, because mine have been very high for a number of years, which are the suppressor cells. I'm just wondering if you've ever used any human beings for trials for vaccine - people with HIV.

Dr. SCHLESINGER: Well, we conduct human clinical trials and there are two kinds of - well, there are many kinds, but in this regard, there are two kinds of trials. One are prophylactic trials, or trials where using the vaccine to prevent people who are not infected from getting infected, and the other are therapeutic trials, where you're using the vaccine to help to stimulate the immune system of people who are already infected. And both kinds of trials have been conducted.

It's generally considered that it is harder to control a virus that's already infected a person, than it is to prevent infection, that it's a higher immunologic bar. But with that said, from the beginning of vaccine development, there has been trials conducted by - frankly, by others. I conduct trials of vaccines for prevention. Colleagues of mine, though, have conducted several clinical trials of what were considered to be promising candidate vaccines in people who were infected, in the hope of helping to modulate their infection.

JAMES: (unintelligible) I heard, I mean, I feel like I should be researched, because, I mean, I'm healthy. My viral (unintelligible)...

FLATOW: What, what brought your disease under control?

Dr. SCHLESINGER: Did you say you were in Boston?

JAMES: I live in, well...

FLATOW: Hyannis?


FLATOW: Yes...

JAMES: Actually, I just returned from - I was in a research study conducted by MIT and Mass General about...


JAMES: (Unintelligible) so I (unintelligible)...

Dr. SCHLESINGER: That's terrific. Thank you.

JAMES: But, and I've asked those researchers there, you know. They think I'm an interesting person, because I've survived, and done so well also. But you know, I'm just curious about whether or not, you know, there are - there's any interest in using people who have survived their blood types. You know, it's some sort of...

Dr. MOORE: Yes, yes, well, there's a major research effort going on in several cities, but near you, at the Massachusetts General Hospital, elite control, a study run by Bruce Walker that is, that actively seeks people with your characteristics to try and learn why you've been so healthy for so long.

FLATOW: Any hints, Dr. Moore, why? There a number of people like him who have...

Dr. MOORE: Well, it's a few percent of HIV-infected people, what's known as long-term non-progressive who are elite controllers, who have - whose immune systems have been able to control the virus, and it's important to understand why that is, and they, in general, have, quote, "better immune systems," and the details of that are incredibly important, and that's what's actively being researched.

FLATOW: What about the other treatments? Are there successful - we've heard for years about the cocktail treatment given to people with HIV. Do we know why they're successful? And how long they work for?

Dr. MOORE: Sure, I mean, the treatment has been the success story of the HIV/AIDS era. I mean, the drugs that are available nowadays are just so much better than the first generation that were introduced in the '90s. There's new drugs approved every year, now with different characteristics, better properties. They work well in combination. They're less toxic. They're easier to take. It's more convenient. So for the people in the States who can afford the best healthcare around, HIV/AIDS is a manageable infection for many, many years. How long that will remain so is yet to be determined by the course of events in the future, but...

FLATOW: But you put a good - you put an interesting caveat on that. You said that people in the United States who can afford it, where it's for people abroad in Africa, it was raging out of control.

Dr. MOORE: Sure, and the issue is getting drugs rolled out into the countries that need them, and that's financial and logistical issues that really are not science in the sense of some - the drugs exist. It's a political and...

Dr. SCHLESINGER: And social, and political, and cultural as well.

Dr. MOORE: It's all of the things that are dealt with by other factions of the HIV community, HIV research and treatment community.

Dr. SCHLESINGER: And those are tremendously daunting problems. The ability to treat the infection, with HIV, is really one of the great scientific, I think one of the great scientific and medical breakthroughs of our time. You know, I was a young doctor in the beginning of the epidemic, and it was like Camus' "Plague." I mean, people came in, young people came in dying, and there was nothing we can do.

And now, people are treated and leading lives of, you know, great promise, and great productivity, and they have to take their medication, and they have to, you know, apply, but, as John said, it's a chronic disease. When you go abroad, when you go to South Asia, or Southeast Asia, or particularly Sub-Saharan Africa, it's like going back to 1985.

FLATOW: Tammy in Grand Rapids. Hi, welcome to Science Friday.

TAMMY (Caller): Hi, thank you for taking my call. I'm a person who lives with, and was exposed to the HIV virus through my partner who eventually died of AIDS, and I never contracted the disease at all. So my question is, why are scientists not studying people like me, who've had chronic exposure, but didn't come down with the virus? And I'm going to take my question off the air.


TAMMY: Thank you.

FLATOW: You're welcome.

Dr. MOORE: Well, again, people who are exposed have been and are sought for research studies. I mean, there are a number of cohorts in the States which do study those reasons and cohorts abroad. I don't know of any studies that are going on in your part of the world, but they surely exist because it is important to find out.

Dr. SCHLESINGER: There's a website from the NIH,, and if you go to that website, there's a comprehensive list of clinical trials going on or relatively comprehensive list. Like John, I'm not aware of the study of what are called highly-exposed but persistently-seronegative individuals in your particular area, but you might be able to find something on that website.

FLATOW: Mm hm. 1-800-989-8255. So the fact that we have effective treatments for people who are infected with HIV, maybe not cheap enough to be able to afford - the whole world can afford to - politically as economically speaking, is vaccination where the attention is now being most paid to?

Dr. MOORE: Well, there's no question that we need the vaccine if we're going to essentially beat the epidemic. I mean, the only way to essentially beat it is to prevent new infections taking place. And the vaccine is the most promising or certainly the most appealing way of doing this. It's also extraordinarily difficult. So it's not going to be achieved for (unintelligible), but it's not time to give up and go home. It's - the benefits are so great that we need to continue to work on this, despite some claims in the press that it's time to give up on the vaccines. It's certainly not, in my opinion.

Dr. SCHLESINGER: I couldn't agree with John more. I mean I think we need to have both a long-term and a short-term strategy, and this is the worse epidemic that hit mankind, a possible exception of the plague. Twenty-five million people have died already, and the reality of it, despite the utility of the drugs, as John said, the only way to end the epidemic just tentatively would be a vaccine, but it's likely a long way off.

So it would seem to me that we need to have a long-term strategy to, as John mentioned earlier, return to basics. As my mentor, Ralph Steinman, likes to say, learn the rules of immunity. Learn how we make a good immune response both from T-cells and antibody, and then apply those rules to make a vaccine. But while we're doing that in our laboratories and in our small clinical trials units, there's an epidemic ranging, and we have to address that epidemic with the tools we have.

FLATOW: And let's talk about some of those tools. One of the more interesting, promising prevention strategies turned out to be male circumcision. Is that an effective tool?

Dr. SCHLESINGER: Yes, it is an effective tool and it's a rather - again, the reason we do clinical trials and we do experiments is because we don't know the answer. But yes, there have been now, I believe, three clinical trials in Africa that have demonstrated clearly that male circumcision is protective, but only partially-protective. And this is part of the great challenge with which we're grappling, that male circumcision reduces the rate of infection of men, depending on the trial, about 60 percent.

So it's not a 90 or 100 percent one we would hope for. But in Botswana or Swaziland, where, you know, a huge number of people are infected in the nine Sub-Saharan African countries with the highest rates of infection, 12 percent of the adult population are infected. And in the most affected countries, it's even higher, like closer to 30 or 40. So if we're looking at reducing that by 60 percent, you're saving, you know, tens or hundreds of thousands if not millions of lives.

But it's not completely effective. So you have to use that and combine it still with education, with voluntary counseling and testing, with condom use, and those are very hard things to do. A vaccine, in its ideal form, you give once and you go home, and the person's protected for life. You know and that's sort of the Holy Grail to which we all aspire. But as John said, it's a long way off.

So how you rule out - you know, imagine asking adult men to be circumcised in resource-poor areas where, you know, even dental work isn't done. And that's a huge logistical, medical, social, political issue and then those men are only partially protected. So one has to be very careful with the communications and the education message so people understand that, and that they still need to use condoms.

And one of the other most effective tools is to reduce the number of partners. So in epidemiologic and social prevention studies conducted by people who do work very unlike with John or I do, it's been shown that that's also one of the most effective tools. So to educate people in that regard is, you know, tremendously sensitive, very difficult, but you know, yet tremendously important in what we have to offer today.

FLATOW: John, you want to chime in?

Dr. MOORE: Yes, and it's important not to forget that it's not uniquely an African or Asian epidemic...


Dr. MOORE: Far, far from it.


Dr. MOORE: In the States, the areas of the community that most would benefit from increased education and increased uptake of antiretroviral drugs are the African-American communities, and there the rates of taking up drugs or the rates of preventing mother-to-child transmission and so forth are much lower than in the rest of America. And that's one of the issues here that we need to address.

It's a distrust of establishment medicine that goes back to many years of distrust of physicians by the African-American community. And one of the reasons, in the HIV/AIDS, area is what Pastor Wright raised when embarrassed Barack Obama recently, the notion that, you know, HIV is a creation of the U.S. government to kill black people, and that, unfortunately, has become a more and more pervasive view, because of the views of Pastor Wright and so on.

And it's instinct to go back to this mess and see where it came from. It was originally a KGB disinformation plot, working with the East German secret police, the Stasi, back in the late 1980s at the height of the Cold War. It was a myth created by the Russians to embarrass America in Africa.

FLATOW: All right, Dr. Moore. I have to jump in and remind everybody that this is Talk of the Nation's Science Friday from NPR News. I'm Ira Flatow, talking with John Moore and Sarah Schlesinger. Let me see if I can get a quick phone call in before we have to go - to Ron in San Francisco. Hi, Ron.

Ron (Caller): Hi. You know this is really interesting. The vaccine is going to be important. But right now, I'm here in San Francisco with the Hope and Beyond's I Am Getting Tested, Are You? Project, which is focusing on all generations, focusing on destigmatizing the disease. And our main concern here for research is, why haven't we really focused on providing a test that everyone can use inexpensively for this reason.

What we call the hidden factor of HIV infection where there are no symptoms or very little symptoms for young people, who are new to sexual maturity, who are in great numbers, who could go for years without being aware that they are infected. We need to drive the testing forward and drive the testing procedures forward, so there's privacy maintained, so we can overcome this disease while research can find a way to create a vaccine.

Dr. SCHLESINGER: Absolutely. What you say is very important, and you remind me, early in the epidemic, the Holy Grail was a test. That was the first great accomplishment, before we even dreamed of therapy or vaccine, was a simple diagnostic test. And to this day, you know, testing is a tremendously important part of any prevention strategy, and there has been, you know, quite a number of leaps forward in terms of testing.

There is now the OraQuick test, which doesn't require blood. It can be done from sort of a scraping inside the mouth. And I believe there's a campaign by the CDC to increase the amount of testing and destigmatize you know getting tested as well, of course, as being diagnosed as positive. But you know, those are hard things to do and I...

FLATOW: No amount of available tests will encourage somebody who doesn't want to be tested.

Dr. SCHLESINGER: Exactly. And you know, again, you get into the realm of behavior and values, and these are very sensitive areas. I mean, one of the great challenges of this virus is that it's associated with behaviors that in some ways are stigmatized. And it's made it more difficult to treat and to prevent for the very reason that you mention.

FLATOW: John, any last words?

Dr. MOORE: No, Sarah is right. I mean, testing is another success story. The tests are 99.8-percent accurate, and anyone who feels that they are at risk of HIV infection should be tested and learn whether or not they need to modify their behavior or go on to antiretroviral therapy. And it's best done in physicians' offices but there are tests that can be purchased from (unintelligible) and other quick tests but still best done in the care of a licensed physician.

FLATOW: Well, thank you both for taking time to talk with us. I appreciate your comments. Sarah Schlesinger, associate professor of clinical investigation at Rockefeller University and the Aaron Diamond AIDS Research Center here in New York. John Moore, professor of microbiology and immunology at the Cornell Weill Medical College of Cornell University. Have a good weekend and thanks for taking time to be with us today.

Dr. SCHLESINGER: Ira, thank you very much.

Dr. MOORE: Thanks, Ira.

FLATOW: You're welcome.

Dr. MOORE: Bye-bye.

FLATOW: Greg Smith composed our theme music. We had help today from NPR librarian Kee Malesky. Surf over to our website at where we're podcasting and blogging and putting up all kinds of new videos. Also a special treat, we're going to be on the road next week in Milwaukee, at the public museum in Milwaukee. If you want to know details, go to Wisconsin Public Radio's website.

Easy to find, Wisconsin Public Radio. Click on the wacky picture of me there on the webpage and you can get information about how to get tickets for seeing us in Milwaukee next week. We'll be talking about Great Lakes and beer. So, what a great combination to talk about in Milwaukee. Stay with us, next week, we'd like to see you in the audience. Have a great weekend. I'm Ira Flatow in New York.

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