Dr. Fauci on 30 years of AIDS

In 1981, I was at the National Institutes of Health. I was a senior investigator and
the head of a laboratory called the lab of immunoregulation, of which I still maintain
that laboratory 30 years later. What we were studying at the time, before the appearance
of the AIDS cases that we first saw then, was the interface between infectious diseases
and the immune system, and particularly the regulation and the disregulation of the human
immune system. I remember it very, very clearly because it
was associated with some major decisions I made about changing the direction of my career.
I was sitting in my office at the NIH Clinical Center, the research hospital where I had
my laboratories, and what came on my desk in June 1981 was the June 5 edition of Morbidity
Mortality Weekly Report, the weekly summary that comes from the CDC. And it was a report
of five otherwise-healthy, interestingly and curiously gay, men who presented in Los Angeles
with an unusual pneumonia called Pneumocystis pneumonia, which is seen only in individuals
who have compromised body defenses or immune system.
I had seen several patients with Pneumocystis, because as an infectious diseases clinician,
I was not infrequently called to consult on patients of the cancer institute who were
receiving chemotherapy and would occasionally get this bizarre type of pneumonia. I didn’t
make anything of the initial report because it just was curious, a little disturbing;
I wasn’t quite sure what was going on. And then exactly one month later, July 4, 1981,
another edition of MMWR landed on my desk, as it does every week, and I read it, and
now this was an additional 26 men, and again curiously all gay men, all previously healthy,
presenting now not only with Pneumocystis pneumonia but also with a strange cancer called
Kaposi’s Sarcoma and other infections, and it was at that point that I fully realized
and knew -- and I actually remember getting goose pimples about it -- “Oh my goodness,
this is a new disease, and it must be a new infection or a mutated form of another infection,”
because it was well known at the time that gay men often got a variety of different infections:
bowel infections, hepatitis, things like that. I didn’t know what it was, but I made a
decision then in the middle of the summer of 1981 that I was actually going to change
the direction of my career and start bringing into the hospital and studying these unusual
situations of gay men who had this strange disease, in fact we used to call it for a
while Gay Related Immunodeficiency, or G.R.I.D., until it became clear that the disease went
well beyond the gay community and involved essentially anyone who would practice risk
behavior that would put them at risk.
I wrote an article in December 1981 that ultimately got published in June 1982 in the Annals of
Internal Medicine. It was a commentary, and in the commentary I stated very clearly, although
we don’t know what this agent, if it is agent, is, that because it is seen almost
exclusively in an epidemiologically restricted population, anyone who assumes that this disease
is going to stay confined to the gay population is making that assumption based on no scientific
data. So be careful because it very likely is going to spread well beyond this. And I
said it, you know, in a commentary. I didn’t have any data; I didn’t have the virus.
It just looked to me saying, here’s an infection, it’s being almost certainly sexually transmitted.
There are a few things in the world that are universal: one is sexuality, the other is
you got to eat and you got to drink, and if you’re going to procreate you’re going
to have sex, and even if you don’t want to procreate you’re going to have sex.
I was following the cases that had been reported, and preparing my lab and my team that I was
putting together, and then when we finally got a small team together, myself and literally
just a couple of other people-- not very many people were interested in studying this--we
began in earnest admitting patients right in the beginning of the year, right around
the Christmas, New Years holiday in 1981-82.
So I got very concerned that a sexually transmitted infection that was lethal, because by that
time it became very clear to me, because all of my patients were dying, that this was something
that we really better be careful of. And it was that kind of concern that made me very
confident that I was making the right decision in turning the direction of my research away
from inflammatory diseases to study this bizarre new syndrome that was appearing among gay
men.
[Well] it was very interesting because, unlike other research projects, the patients who
came in to see us were very advanced in their disease and I spent as much or more time as
a physician taking care of the patients as we did doing classical bench research. So
it’s an interesting phenomenon, notwithstanding the intensive amount of time we had to put
in to take care of them. But at the time my lab was a laboratory that had been studying
aberrant B cell function, B lymphocyte function, in people with different types of hypersensitivity
or autoimmune diseases, so we were expert, as it were, on looking at abnormalities in
B cells and in T cells.
So even though we suspected it was a virus, in fact we were sure it was a virus, we didn’t
know what virus it was. We looked phenomenologically at what was wrong with their immune system.
So we began studying their T cells and their B cells, and from my lab we made some of the
earliest seminal observations that this disease was characterized paradoxically by an aberrant
immune activation even thought it was an immuno-deficiency disease. And the first paper that we published
in the New England Journal of Medicine in 1983 made that observation that isn’t it
curious that their B cells that really are not -- we didn’t even know which cells were
infected or not because we didn’t even know what infection it was -- but their B cells
were hyperactive and yet they did not function very well. And that was our statement back
then, that isn’t it curious that this is a disease of hyperactivity of the immune system
at the same time as it’s an immuno-deficiency. And then in the following year we pinpointed
the very nature of the T cell defect, one of antigen-specific T cell defect.
We did that for a couple of years and then when the breakthrough from other labs -- from
Montagnier in Paris and from Gallo in the United States--once we got the virus in our
hands, namely in 1984 and 1985, then we began to study in earnest some of the pathogenic
events, and from then until this very day we study the pathogenesis of HIV disease both
in treated and untreated individuals.
[well] the first cases were in summer of 1981. The paper from Montagnier that showed the
famous electron micrograph of the virus in people with this lymph node enlargement, that
was in May, 1983. And then a year later, in May, 1984, Gallo showed the absolute connection
between the virus and the disease. So it was two to three years following the initial observation.
/
When Bob Gallo proved that it was the etiologic agent in 1984, we had a diagnostic test approved
by the FDA in 1985, so the test was developed, it was gone through the appropriate validation,
and approved by the FDA. That was really quick, from literally less than a year from the time
that it was shown to be the virus that causes this disease. We started off with an antibody
test that’s a very sensitive test. It’s confirmed by what we call a Western Blot test
for diagnosis. It’s very easy to do. Several generations later we have tests that can be
done literally in minutes, could be done on saliva, could be done on blood. But the molecular
techniques to probe for the virus, PCR and a variety of other techniques that we now
have, are widely used throughout the world, and they’re very sensitive and very good
tests for the virus.
[Well,] there are a couple of aspects about HIV that are very unique and extremely frustrating
with regard to the fact that you can’t -- not only can the body not spontaneously eradicate
it, but you can’t eradicate it with drugs, even though you can effectively treat a person
to the point of allowing them to lead a relatively normal life by suppressing the replication
of the virus. But what the virus has is multiple characteristics, probably the two most important
of which are that A, it mutates very rapidly. It’s an RNA virus, it replicates at an enormous
rate, and it mutates. So the body’s immune system is constantly trying catch up with
it and essentially never does. It partially suppresses, but certainly never completely,
with very few exceptions in a group of patients called elite controllers, but that’s less
than one percent of the people that are infected.
The other thing is that it’s a retrovirus, so it integrates itself into the genes of
a cell and it hides there in what we call a reservoir. So there are infected cells that
are not being seen by the immune system. The other thing is that the part of the virus
that would induce a response that would be able to suppress and protect you, namely a
neutralizing antibody, is hidden from open view of the immune system; that is, the conformation
of the virus protects that critical part like the part that binds to the molecule on the
CD4 cell, that’s shielded from the body’s immune system and only recently, over the
last year or two, by using structural biologic techniques, have we been able to get a handle
on that very important component of the envelope, or the outer coating, of the virus, to be
able to start making intelligent, structure-based, vaccine designs.
Did anything surprise me? Well, yes, everything surprised me about it because it was the first
time a retrovirus that replicated…I mean HTLV-1 was discovered by Gallo as a cause
of T-cell leukemias in the ‘70s, but it wasn’t a virus that was destroying cells,
it was inducing a tumor. What surprised me about HIV was its recalcitrance to being able
to be suppressed, and most surprising was the curious observation that is true today
of how the immune system just cannot handle this virus. If you look at any, even the deadliest
historic scourges -- the Bubonic Plague, which is a bacteria, but smallpox as a virus, polio
as a virus, measles as a virus--all of those, even though they had a considerable degree
of morbidity and some mortality, at the end of the day, the body proved the concept that
it could ultimately suppress the virus, eradicate the virus and leave you with lifelong protection
against reinfection. That didn’t happen with HIV. So if you asked me, of what the
one thing that surprised me, shocked me and scared me a bit, was that here was a virus
that the immune system just was not particularly challenging to this virus. It suppressed it
a little but the virus always won the battle against the immune system.
Research into treatment began immediately, immediately after the virus was isolated.
So as soon as the virus was isolated we began, here at NIH, screening drugs that were already
on the shelf for other reasons, as well as the beginning of what’s called targeted
antiviral, where you delineate all the functions of all the genes of the virus and see if you
can specifically block those functions by molecules that you would develop to specifically
block it, but that took a while. In the beginning the only thing we had was this virus replicating
in a culture. So the first approach was screening molecules, and that’s what the contribution
of people like Sam Broder and Burroughs Wellcome were, because what they did is they screened
a whole bunch of molecules and one of them, AZT, which later became zidovudine -- AZT
is a reverse transcriptase inhibitor that was originally developed for the treatment
of cancer and wasn’t a particularly good anti-cancer drug. When that drug was screened
it blocked completely HIV, and then it went into the preclinical into a clinical trial
and that’s how we had the first clinical trial of an AIDS drug. And that’s how AZT
got approved in 1987 by the FDA.
It was tough in the beginning. I had considerable resistance from people trying to discourage
me from directing my own career toward this. I had some mentors who would say, why are
you wasting your time on this disease that’s involving a very well-defined group of disenfranchised
people? As the time went by, when I began to push for more resources with the Congress,
with the administration, with the secretaries, with all the people I dealt with to try and
convince them to do more, it was a mixed response. Some people heard what I said and said “I
understand it is going to be something bad, we’ve really got to go after it.” And
other people did not. And it really depended upon who you were talking with and what their
other interests were. I know in the infectious diseases community there were individuals
who thought that we were overdoing it. I developed a special division of AIDS here at the National
Institutes of Health, and there were some of the classical infectious diseases people
who, quite frankly, felt very offended at that and were…made their thoughts and their
feelings known about that, thinking I was over-emphasizing a disease that was only affecting
a few thousand people. / 1:23:08.10 They’re no longer here, but unfortunately my instincts
were proven to be correct, and that’s unfortunate, because we know we now have had 30 million
deaths from HIV and 33 million people living with HIV infection.
[Well,] in 1984 when the position of the director of NIAID--National Institute of Allergy and
Infectious Diseases--opened, I never really had an interest in administration. I was fundamentally
a bench scientist and also a clinician who is trained in and practiced both infectious
diseases and clinical immunology. But it became clear to me that particularly with AIDS, but
also with other emerging infections, and the gradual evolution of our interest in global
health and the impact of infectious diseases on global health, I thought I could have greater
impact on the field if I took on the added responsibility of running the institute. It
wasn’t a stopping of my research and stopping seeing patients, it was -- I took it under
that condition that I would also be able to continue to do my research and continue to
see patients.
The secretary agreed to that, the director of NIH agreed to that, and that’s what I’m
doing right now. I’m not only continuing as a scientist and as a clinician but I also
now have the responsibility for the broader research with an institute that’s primarily
responsible for most of the infectious diseases research, including HIV/AIDS, in the world.
[Yes,] I was very transparent and upfront about our needs. We didn’t always get what
we wanted, but I tried to articulate as best as we could to the Congress and to virtually
every president since Ronald Reagan I’ve had the privilege of being able to interact
with, speak with, on more than one occasion depending on the president, starting off with
President Reagan, very intensively with George H. W. Bush and very intensively with President
Clinton, and then really quite intensively with George W. Bush, particularly in the development
of the PEPFAR Program, which he asked me to help put together for the country and for
his presidency, which ultimately became the President’s Emergency Plan For AIDS Relief.
And also with the current President who, as obviously we all know, has a very intense
interest in global health.
With the Congress, we’ve been very fortunate to have bipartisan support for the AIDS effort
in every Congress that I have interacted with since the summer of 1981 up until this current
day right now. In the early years, it was interesting because sometimes you would see
where you would have a split government with a Republican president and a Democratic congress,
or a Democratic congress and a Republican president, vice versa, that you would often
see some tension back and forth, but for the most part, even though sometimes the hearings
got a little tense, at the end of the day the support for HIV research was always there
both on the part of the Congress and on the part of the administration.
SLATE: THE ROLE OF ACTIVISTS
[Yes,] very early on in the course of this pandemic, the activists were making extremely
good points about the uniqueness of this, the need to do more, the need to be less rigid
in our regulatory approaches towards the approval and testing of new drugs, and the rigidity
and lack of flexibility in how we designed clinical trials. All of which were the classical
way to approach drug development, therapeutic developments, clinical trials and FDA approval.
They wanted to get our attention, so they would do it in a very theatrical way, and
they scared a lot, because for the most part the scientific community and the regulatory
community are conservative. And when I say conservative, I don’t mean conservative
in an ideological, political way, but conservative in their approach toward science. It’s nice
that people are interested who are not scientists, but leave them out of it and lets us scientists
make the decision. So they didn’t pay much attention to the activists. I, for one reason
or the other, began reading intensively what they were writing, and even though when they
were demonstrating and closing down Wall Street and invading St. Patrick’s Cathedral, and
doing things like that, looking very eccentric and scary to some people, I tried to phase
that out and just listen to what they said and read what they wrote and they were making
perfect sense. So since I was always out there as a government official, they equated me,
my face, my name, with the Federal Government, so they began to demonstrate against the NIH.
And right here on our campus they, you know, came and invaded the campus, smoke bombs,
wanting to get arrested, and I made probably the best decision in my interaction with the
community, is that I agreed with what they were saying, so I went downstairs outside
when they were all over the lawns and all over the property, and they were getting ready
to be mass-arrested, and I told the Montgomery County police, “Don’t arrest them, just
get five of the leaders or more and bring them to my conference room” --in fact where
we’re sitting right here--“and have them come up and talk to me.”
They were shocked, the activists, no one had ever spoken to them; the only thing they ever
did was to try and get them arrested. We spent a couple of hours talking about how we could
work together, and how, even though much of what they said was correct, a lot of what
they said was not correct. So they learned from me and I learned from them, and ever
since then we have had an extraordinary relationship with the activist community. They’re on
our advisory boards, on our clinical committees, on our community committees. It’s become
an extraordinary partnership.
[Well] there was no doubt that the persistence, energy, and articulate way that many of the
well-informed activist community was able to make their point, had a significant influence
on the funding of HIV/AIDS. There is no doubt about that.
To my knowledge there has never been this type of activism. The AIDS activism was unique,
it was effective and it has now spawned activists. They’ve almost written the book on activism
now so other diseases, though they are different diseases with different circumstances, without
a doubt look toward the AIDS activists and say, how do we get done what they got done?
In fact I’ve explicitly had people who are advocates for diseases that I have nothing
to do with, no responsibility, no special expertise in, who’ve come to me asking the
same question that you’re asking; namely, tell us about the activists about their impact
and their influences on you and on the process. Because they want to mimic that for their
own diseases.
Whenever you have a person who’s well-known and well-respected like a well-liked actor,
like Rock Hudson, a very popular sports figure, like Magic Johnson, that the world -- those
in the world, those in this country who had a bit of a stigmatization approach toward
HIV infection, particularly those who are not used to interacting with the gay community
or with others, when they saw someone who they admired for other reasons and found out
that they were HIV infected, even if they were a gay man like Rock Hudson, they would
say, well you know this disease, you know, really attacks anybody, and maybe I should
just drop back a few yards and get rid of the stigma. So I think that the infections
and the coming out of people who are well known, particularly in the entertainment and
sports industry, went a long way to get people’s attention, but also to get rid of some of
the stigma associated with HIV.
Dr. Koop was a close friend. I was his personal physician. Still am -- well, I'm not “still
am.” I am. He calls me up every once in a while, but he's geographically no longer
here. He's in New Hampshire. But when he was being chosen for the Surgeon General in the
Reagan Administration, he came down to Washington, and there was a lot of opposition because
people thought he might be too conservative. So he spent months and months and months being
led on a string of multiple hearings with no confirmation as Surgeon General. And he
was getting very, very, anxious about it. He was getting stressed and his blood pressure
was up. So I was the person on campus here who was generally the internist for the doctors
who got sick, because I was practicing medicine as opposed to just doing research with no
medical connection. The Surgeon General -- some people don't appreciate it -- lives on the
campus of NIH, in a house literally 100 feet from my office, where I am in the administrative
building now. So, he was told to come and see me. I took care of him. And I joke around
with him a lot about it, and I've said it publicly many times. After a classic big workup
that I gave him, my diagnosis was the “Welcome to Washington Stress Syndrome.” And that's
what he had. And once he got approved and confirmed, our friendship grew.
He didn't do AIDS in the beginning, but then he decided this is a big problem. And when
he would come home in the evening, he would walk by the building that I'm in to get to
his house, and very frequently, he would come up and sit down on the couch. Sit down, relax,
you know. Have a glass of water or a Coke or something and talk about HIV/AIDS. And
then he decided he was going to go ahead and do something about it. Then, thus came the
Surgeon General's Report and the letter to all the households. He taught himself about
AIDS and had hours and hours and hours of conversation with me about it, because that
I was doing almost full-time. So, we are still friends to this day. We have a very good friendship.
It was a very interesting process. AZT became available in 1987. We were all very optimistic
about it, but our optimism was short-lived, and then we had the cold, sobering, realization
that we were in it for the long run because individuals who improved, I mean the first
study, comparing AZT to a placebo -- in the AZT group there was one death, in the placebo
group there was 19 deaths; it was 19 to one. So it was very, very clear that it was effective,
but when you started using it literally months, usually, sometimes longer, the virus did what
you’d expect the virus to do. It mutated and then AZT as a single mono drug was no
longer effective. …the next drug didn’t come out and be
approved by the FDA for another couple of years after that, and then you had drugs that
were used individually, and then two at a time, and we did that for a few years until
we got to the early to mid 1990s when the protease inhibitors were discovered, again
by targeted drug development. Crystallizing the protease enzyme and figuring out what
molecule you could develop that would block that. And the first protease inhibitors came
out, a clinical trial was done with three drugs including a protease inhibitor, and
the results were stunning: the virus level plummeted to below a detectable level. And
then of the years from 1996 to the present, even better and better drugs were used: non-nucleoside
reverse transcriptase, better generation protease inhibitors, nucleoside reverse transcriptase
inhibitors, integrase inhibitors, inhibitors of binding and fusion of the virus. So now
we have more than 30 drugs that are approved by the FDA, that when used in combinations
have a striking dramatic effect on suppressing the virus. So from 1996 until the present,
we just did better and better and better with regard to drugs.
We started working on a vaccine literally right after the virus was discovered. We got
a component of the envelope and we used the envelope expecting, somewhat naively like
with any other virus, get the outer coding and inject it into somebody, they’ll make
an immune response that was protective. And it was the first years of realizing that by
injecting the outer covering of the envelope; the GT-160, the GT-140, the GT-120, any of
that into an individual induced an immune response, but the immune response was not
protective. We started that like, right after like ‘84, ‘85, ‘86 was the first time
we did it. You know, the first vaccine trial officially was started here at NIH in 1987,
which was just three years after the virus was discovered.
I could tell you exactly what the origin of the Vaccine Research Center was. Dr. Harold
Varmus, who was the NIH director at the time, and I visited President Clinton in the oval
office because he and Vice-President Gore wanted a little background and briefing on
HIV, so I had the opportunity to brief them on various aspects and clinical issues with
HIV. And as we were walking out of the oval office the President asked us, “What is
it that you really need right now?” I said, “Well, we certainly desperately need a vaccine,”
and “How could you get a vaccine more quickly? What could we do?” And we said what we really
need is a center that’s entirely devoted, from basic science up through the clinical
trials, to develop a vaccine, and when the President decides he wants to do something
it gets done. And he just said, “Fine, let’s do a vaccine center at the NIH.” And that
was it. And very, very quickly it went up and now it’s really one of the prize scientific
centers here at NIH.
[Well] we have, for the first time a year and a half ago, a vaccine. We started the
first trial in 1987 and we had 23 years’ worth of disappointment until last year, a
year and a half ago, when the Thai trial, which is referred to as RV 144, in 16,000
individuals in Thailand, showed the first signal of efficacy. It was only 31 percent,
not enough for primetime, but enough to prove the concept that you could actually get a
vaccine that would prevent acquisition of infection.
Since then we have been very, very energetically pursuing vaccine development with a number
of important new discoveries, namely the monoclonal antibodies that people rarely make, that are
antibodies that identify a component of the virus that actually would induce a broadly
reacting neutralizing response, and now by using structure-based vaccine design, we’re
doing the same sort of design of vaccine using structure as our tool as we did years ago
with drugs, when we used the various components of the virus as targets for drugs, we’re
doing the same thing in a structure-based vaccine design.
[Well,] in my own lab, we're still involved in the pathogenesis of HIV infection. We're
studying the reservoirs of HIV, which is aimed at trying to develop a cure for HIV, to be
able to delineate better that small, recalcitrant reservoir. Is there any way we could get rid
of that reservoir, either immunologically or pharmacologically? That's one component
of the research. The other -- as we've been fortunate enough to find and discover -- a
new receptor for HIV that plays a major role in the transmission across mucosal barriers.
And that is steering in the direction of vaccine development.
[Well] I think that the whole study of HIV was a big boost not only in the study of any
kinds of viruses: the molecular approaches, the ability to do high-throughput sequencing
and get various versions of what we call the quasi-species, or the different components
-- it isn’t one virus that’s uniform. It’s what we call the quasi-species, which
means that there are multiple subtle changes that exist, almost like in a swarm of viruses,
as opposed to one identical virus that you have millions of copies of, there are millions
of copies of different types of modifications of the virus, so -- but a lot of other disciplines
benefited from the study of HIV, even our understanding of the immune system and the
fact that the regulation of the immune system is a very complex, interdigitated process,
that was, by an experiment of nature, in this case the experiment was the infection of the
human species, with this virus, has allowed to be able to delineate much more precisely
many of those circuits of regulation of the immune system.
[But even more importantly,] vaccine is going to become part of a combination prevention
approach. We already have within our grasp the tools, if fully implemented, to really
turn around the AIDS pandemic. We have very effective prevention modalities from behavior
modification to condoms, needle exchange, mother to child transmission, circumcision,
topical microbicides, pre-exposure prophylaxis, and the more recent, dramatic, game-changing,
observation that was made very recently from an NIH study, that was a multinational study
but sponsored by my institute, was what was called HPTN052, which was the trial that showed
that the earlier you treat an infected person compared to waiting a little bit ‘til their
disease progressed, not only do we have what we already know is a beneficial effect on
the infected person, but a dramatic, truly dramatic, decrease in the likelihood that
that person will transmit the virus to their sexual partner. And that is a game-changing
study which proves that treatment itself can serve as a form of prevention.
Well if you compare the people who receive therapy early, namely right at the beginning
of the study, the chances of their transmitting virus to their sexual partner compared to
the people who delayed therapy ‘til when they got to a certain point, there were 28
linked infections. 27 of them occurred in the people who delayed their treatment in
their sexual partners, 27 of the infections of sexual partners versus one infection in
the people. That is a highly significant effect of a 96 percent decrease in infection.
We have a component of our large AIDS clinical trials network, is the prevention trials network.
So if you consider vaccine as prevention, we have a substantial -- at the NIH -- half
a billion dollar per year vaccine effort. More than that, actually -- close to $600
million. But in prevention, we have a number of things. We have behavioral modification,
promotion of the use of condoms. The mother-to-child transmission study was funded by NIH. The
topical microbicide study was done at NIH sites, together with USAID. The circumcision
study was sponsored by the NIH. The pre-exposure prophylaxis study was sponsored by us. And
the most recent, very important treatment-as-prevention study is funded by us. So we have a very extensive
portfolio in prevention.
Well, very, very early on because with -- there was a project called “Project SIDA,” which
was in Kinshasa, in the former Zaire, now the Democratic Republic of the Congo. And
we sent down an individual, as did the CDC, as did the University of Antwerp. And the
sort of interesting thing was one of my people that we sent down there was Tom Quinn, who
is the Associate Director for our International AIDS and STD work. 2:03:00.80 The person who
was from the University of Antwerp was Pida Piat. And the people from the CDC was Jonathan
Mann, when he was down at the CDC. And their experience in Kinshasa was totally different
from what we were seeing here in the United States. And it was there that they realized
that this was a 50-50 proposition, men and women. And it was overwhelmingly heterosexually
transmitted. And then, as the years went by, when we were able to partner with a variety
of southern African countries, it became clear that this was an overwhelming problem in southern
Africa. But the first hint of it, literally, came from the studies that started in Project
SIDA.
[Well,] PEPFAR is the President's Emergency Plan for AIDS Relief. And it got started in
an interesting way. During the George W. Bush administration, President Bush sent Tommy
Thompson -- who was the Secretary of HHS at the time -- and I, together with the group
that the Secretary was bringing down, on a fact-finding mission to various African countries
to scope out what was going on down there. And when we came back, he asked me to put
together a mother-to-child transmission -- because it was just then that Nevirapine was shown,
in a single dose to the mother, followed by a single dose to the baby right after birth
-- mother during labor, baby right after birth -- had a major impact on blocking transmission
on mother to child. We came back and I made a proposal to the president, with the help
of his staff, who at the time was Josh Bolton and Gary Edson and Jay Lefkowitz and Margaret
Spelling and others -- that a $500 million investment in mother-to-child transmission
would be a very important contribution.
After I presented it to him in the Roosevelt Room, as I was walking out of the room, he
grabbed me and grabbed the -- Josh Bolton-- and said, “I want you to go back and make
it something much bigger. I want a game changer for Africa. I want you to go and get multiple
models, and come back, and work with the staff to see what we can to do to really turn things
around in Africa. I want it to be feasible. I want it to be implementable and I want it
to be accountable. I don’t want to just give money to foreign countries and say, 'Go
do it.'”
So, that was in April, when I went the first time. And then from June of 2002 -- that was
April 2002. From June 2002 until December 2002 and January 2003, I went back and forth
with the White House, of trying to get the right model. How many countries, how could
you get the maximum number of people, can you include 50 percent of all the people in
the developing world infected, should you include India, should you include China, should
you include the Caribbean? Model it out. What would it cost, how much on treatment, how
much on prevention? 2:06:19.10 And it was really almost a full-time job back and forth.
I employed a person who was first a fellow in my lab, but then became my assistant for
a while, who was interested in helping. His name is Mark Dybul -- who actually turned
out, ultimately, to become the Ambassador in charge of the program after Randy Tobias
left.
Make a long story short, we weren't sure that they were going to accept it, because there
were a lot of people -- particularly the people who take care of the money, OMB and others--who
were not enthusiastic about this plan that I put together, that was $15 billion over
five years. But I had the encouragement of the president, the encouragement of Josh Bolton
and others, particularly people who most people don't ever hear of but were White House staff
who were very helpful -- and Gary Edson and Jay Lefkowitz and others. And we put the program
together, and I didn't know whether it was going to be accepted until the very beginning
of January, when they called me down to the White House and said, “Let's figure out
a couple of paragraphs to put into the State of the Union Address on January 28, 2003.”
And I just said, “Oh my God. It's going to happen.” And it did. And it's been extraordinary,
watching it evolve over the years.
The impact is enormous. It's historic, with regard to the United States of America's impact
on a global health problem. It was the largest program devoted to a single disease in the
history of our country. Right now, if you look at the numbers, there was over three
million -- between three- and four million -- people who were on antiretroviral therapy.
There's -- you know, hundreds of thousands of babies have been saved from getting infected.
Millions of people have been put under care. And it's still going strong. I mean, PEPFAR
is the showcase of the United States' AIDS effort throughout the world.
Now it's part of President Obama's broader global health issue, so it's even taking a
bigger impact now, because it's being linked to other global health problems.
There is an urgency of a different type. Back then, it was an urgency of discovery, of getting
drugs, of treating, of preventing. Now, it's an urgency of implementation, where it's very
frustrating because you have so many of the tools -- of treating people, of preventing
infection -- but the logistics and the resources available … it's a tough time right now.
And there is a lot of feeling of urgency, “We've got to do this because the impact
could be enormous.” We could actually get our arms around this pandemic and not only
slow it down, but actually stop it. It would take a global commitment of resources that
don't seem to be available right now.
There are still 2.6 million new infections a year, globally, 56,000 new infections per
year in the United States. It is still a very bad, very unfortunate thing to get HIV-infected.
Just because that there are drugs available is no reason at all to think that, “Oh,
it's okay to get HIV-infected.” It's not. It's a very serious disease. Even at best,
you have to be on drugs that have some toxicities. Sometimes individuals have considerable toxicities
to drugs. Right now, we hope to cure it. But right now, it means you have to take medications
for the rest of your life. So just because we've been very successful, we've got to make
sure that success is not associated with complacency, because then we'll never get out of the situation
we're in right now. The only way to get out of this is to stop new HIV infections. And
you're not going to do that if people are complacent.