♪ ♪ NARRATOR: It began as a mysterious plague.
CECILIA CHUNG: I was doomed to not live very long.
MAN: People are not realizing how bad a disease it is, and there's no cure for it.
NARRATOR: A ferocious killer that frustrated scientists at every turn.
JOHN MASCOLA: If we look at all the viruses that we understand, H.I.V.
is far on the spectrum of difficult.
NARRATOR: But a long, worldwide scientific quest has provided a string of spectacular discoveries.
MYRON COHEN: The science that's developed is, is, remarkable.
NARRATOR: And after four decades, it's led us to the brink of what was once unthinkable: the end of H.I.V.
MONICA GANDHI: We have prevention, we have treatment, and we have testing.
WOMAN: There we go.
NARRATOR: As scientists chip away at the virus's defenses... MICHAEL SAAG: I'm just overwhelmed at the progress that was made.
NARRATOR: ...a once-insurmountable foe is finally on the ropes.
I think we definitely have the tools to end the epidemic in the U.S. NARRATOR: The U.S. government has set a bold target: cut new infections by another 90% by the year 2030.
But can we conquer the last mile and the landmines of accessibility and stigma that lie along the way?
"Oh, he's H.I.V.-positive.
How did he get it?"
TOMMY WILLIAMS: It's just going to take a true collaborative effort.
NARRATOR: "Ending H.I.V.
in America," right now, on "NOVA."
♪ ♪ ♪ ♪ ♪ ♪ Hey.
This is Tommy from U.A.B.
WILLIAMS: It's a lot of time in the clinic, meeting patients, especially for the initial appointments.
Well, I'll see you when you get here, lovely.
NARRATOR: This phone is a lifeline for 2,000 people infected with H.I.V.
who depend on the 1917 Clinic at the University of Alabama at Birmingham.
care, which includes treatment and research, community engagement.
We also do H.I.V.
NARRATOR: Tommy Williams is in charge of connecting patients with all the clinic has to offer.
I can help you with that.
I can help you with that before you leave.
♪ ♪ NARRATOR: In the United States, more than one million people are currently living with H.I.V.
But the burden is not felt evenly across the population.
As they've been since the outbreak began, men who have sex with men are by far the most affected.
(talking softly) Men who have sex with men make up, like, two to three percent of the U.S. population, and they make up about two-thirds of H.I.V.
One is because, anal sex, you have higher risk of getting H.I.V.
just because of trauma and the type of cells that are in that area.
(card reader beeps) NARRATOR: Latesha Elopre, an infectious disease specialist at the 1917 Clinic, says another key factor is stigma.
We saw each other last time.
ELOPRE: There's still a lot of stigma related to H.I.V.
And I think that's also a huge barrier why people don't always access our preventative services or come in to get tested.
♪ ♪ NARRATOR: Race is another risk factor.
Compared to their white counterparts, the lifetime infection risk for Black men is six times higher.
For Black women, it is nearly 12 times higher.
One reason patients are willing to put their trust in Tommy Williams is that he knows where they're coming from.
He's born and raised here in Birmingham... We're on the east side of town.
NARRATOR: ...and he's H.I.V.-positive.
WILLIAMS: There are times when I visit a patient at bedside and me disclosing changes everything.
Like, something grows.
Something beautiful grows.
I became aware of H.I.V.
I think I was in the ninth grade, and, um...
This girl was, like, "He's a sissy."
And then, so these guys was, like, "You fruit loop, "you're a fruit loop, you got AIDS.
You got AIDS."
I wanted to believe that I did not, but I also believed that if I didn't have AIDS, it was just a matter of time.
I was, like, "I'm, this is going to happen to me and, um, and I'm going to die from it."
So, you know, one day, that day came.
NARRATOR: Tommy was fortunate to contract H.I.V.
at a time when highly effective medications offered him a chance at a long, healthy life.
You can live, and I'm living, I'm thriving.
Oh, my God.
I'm so sorry I'm late for this appointment.
NARRATOR: It was a surprisingly difficult road to get to this point.
The treatments available to Tommy are revolutionary, and the result of a decades-long battle against H.I.V.
that never quite went as planned.
♪ ♪ San Francisco has been an epicenter, for both the disease and innovative treatments.
GANDHI: Good to see you, Donna.
Good to see you.
Come on back.
NARRATOR: Dr. Monica Gandhi heads up Ward 86 at the University of California, San Francisco, the oldest dedicated H.I.V.
treatment unit in the world.
I can see your light reflex in that eye.
GANDHI: I always knew about Ward 86.
It was just in my head, and I just wanted to be here.
I wanted to be a part of this.
And then in 2014, I became the medical director of Ward 86, which has been really a privilege.
DONNA: In 2004, when I had AIDS, I asked God to just help me to live with it.
And I've been doing just that.
NARRATOR: When Ward 86 first opened in 1983, an AIDS infection was a death sentence.
Cecilia Chung arrived in San Francisco in the early 1980s to escape her strict Hong Kong family and to sample life as a young gay man.
But she found a scene much different than what she'd pictured.
CHUNG: When I tried to, like, go on my adventure, I would see maybe five or six people in one of the bars, and it didn't take long for me to figure out what's going on.
People were avoiding talking about it, but everybody knows that if you haven't seen your friends for more than a week, chances are you never see them again.
So this is Divas.
CHUNG: When my mom came visit, my mom say, "Don't sleep with men, you will die."
So I never expected to live past 30, and lo and behold, I contracted H.I.V.
when I was 27, 28.
It was called gay cancer and GRID-- Gay-Related Immunodeficiency.
♪ ♪ NARRATOR: In May 1982, when "The New York Times" reported on so-called GRID, it stated, "Epidemiologists have found no evidence "that the condition is spread from person to person "like influenza or measles.
The general public need not fear an epidemic."
♪ ♪ It wouldn't take long to see that confidence was misplaced.
By the early 1980s, cases of the mysterious illness were appearing in cities all over the country.
♪ ♪ (knock at door) Good afternoon.
SAAG: We were seeing more and more people, especially from outside of Birmingham, coming in to see us.
And you could just feel the epidemic beginning to crash on our shores, if you will.
NARRATOR: In Birmingham, Mike Saag was just two years out of medical school when he saw his first case.
I remember were thinking, "This is really unusual."
This guy was in his early 30s.
He had no reason to be sick.
Something was desperately wrong with the immune system.
ELOPRE: Any disease that we've encountered in history as an infectious diseases provider, the key has been to, number one, identify that disease, to learn and effectively treat that illness.
And then the biggest, the way to stop pandemics, is to prevent it from being spread.
So, immediately, all of our attention begins to focus on this causative agent.
NARRATOR: Scientists around the world began a frantic search for clues.
And in the spring of 1983, they found the culprit.
In the cells of sick patients, scientists at the Pasteur Institute in Paris discovered the virus that would come to be called H.I.V.
They found it in CD4 cells, a type of white blood cell that's critical to the immune system.
They would come to know it as a formidable enemy.
Like other viruses, H.I.V.
works by hijacking the machinery of the body's own cells.
By inserting its own genetic material into the DNA of the host CD4 cell, it reprograms the cell to produce the seeds of its own destruction, churning out more and more copies of the virus until the cell bursts open.
SAAG: It turns that cell into a virus factory that then go into the bloodstream and start infecting other cells.
And that's how the infection takes root.
NARRATOR: It's a powerful two-punch combo: rapid replication and weakening the immune system, killing the very cells that are meant to defend against it.
When first infected, patients usually experienced a brief, mild illness.
Nothing that would signal a serious disease.
The patient recovers.
But the virus stays active, steadily multiplying, and killing more and more CD4 cells.
SAAG: That relentless replication ultimately damages the immune system and leads to the opportunistic infections that we see every day, what we would then call AIDS.
NARRATOR: "Acquired Immunodeficiency Syndrome" left the body unable to fight off most infections.
With the virus identified, the race was on to find a treatment.
And in 1987, there came what looked like a breakthrough.
Hope for AIDS patients: the drug AZT.
NARRATOR: As scientists discovered, AZT, a drug originally developed to fight cancer, was able to attack the virus at a key vulnerable point.
is what's known as a retrovirus, only the third to be found in humans.
A retrovirus's genetic material is single-stranded RNA.
To hijack the cell's machinery, it must convert that to double-stranded DNA, like the rest of the human blueprint.
The virus uses an enzyme called reverse transcriptase to make that conversion.
AZT inhibits that enzyme, preventing the RNA from being converted.
In a quickly organized clinical trial, AZT stopped the disease in its tracks.
CHUNG: People were looking for a vaccine and a cure.
So when AZT came out, it offered some hope to us.
NARRATOR: But that hope was short-lived.
It didn't take long for us to realize that AZT is not going to cure us.
LAWRENCE COREY: It became very clear that people who responded to AZT, after three or four or five months, started to lose their CD4 T cells and started to lose weight again, and not gain weight, and started getting, uh, infections again.
NARRATOR: Larry Corey was one of the first researchers to specialize in H.I.V.
COREY: It was perceptually worse, because you got better, you were optimistic you got better, and then you got worse.
MAN: I've pretty much accepted the fact that I'm going to die.
NARRATOR: As scientists studied the virus, they began to understand how it was able to evade the medication.
ELOPRE: The virus can mutate, and that was one of the biggest issues that we had.
The virus can change itself and basically change in a way where that medication stops working.
NARRATOR: Drug resistance is driven by mutation, and H.I.V.
's capacity to mutate is exceptional.
In fact, in the body, H.I.V.
mutates faster than any other virus or any life form that scientists have ever measured.
COVID, or SARS-CoV-2, there's mistakes made, but it has a correction enzyme.
So it has a proofreader that comes through, and if it sees a mistake, corrects it.
doesn't have that enzyme.
NARRATOR: Without the proofreader, the virus churns out different versions of itself-- variants.
does that more frequently than any other virus.
NARRATOR: So many mutations means a greater chance that the virus will change enough to elude the treatment.
GANDHI: It's very wily, it's very prone to change, and it essentially just evolved mutations that made it evade AZT.
's shapeshifting was also sabotaging efforts to create a vaccine.
The work began in the '80s with fanfare and hope.
We hope to have such a vaccine ready for testing in approximately two years.
SAAG: Margaret Heckler, who was the secretary of HHS, had a press conference, and this is around 1985, and she said, "Within two years, we're going to have an H.I.V.
NARRATOR: But the reality of the challenge quickly set in.
Vaccines are designed to trigger an immune response, pushing the body to produce proteins called antibodies, which attach themselves to invaders and tag them for destruction.
It's a tried-and-true approach, used to create vaccines that eliminated smallpox, measles, and polio in the U.S. ♪ ♪ COREY: You make antibodies so that when you get exposed to that agent, one's body recognizes it and therefore eliminates it before it causes any disease.
It prevents you from getting sick.
NARRATOR: But with H.I.V., the challenges were unprecedented.
Most antibodies bind to and block only a single target, a specific surface protein on a virus.
But with H.I.V.
mutating so rapidly, that target was constantly moving.
Working on the early vaccine trials, John Mascola saw the problem firsthand.
MASCOLA: Those proteins surfaces, they change.
So an antibody that sees one strain of H.I.V.
doesn't necessarily see another one.
So there's all this diversity of H.I.V.
in the world.
NARRATOR: The number of variants is stunning.
A vaccine must protect against all of them.
MASCOLA: I think there was a sense of realism that set in that said, "If we look at all the viruses that we understand, H.I.V.
is far on the spectrum of difficult."
Making a vaccine was gonna be a pretty major scientific obstacle.
NARRATOR: A decade into the pandemic, there was still no vaccine, no cure, and no long-term treatment.
Behavior changes, like using condoms, had slowed the pace of new infections.
But the death toll kept rising.
♪ ♪ SAAG: H.I.V.
had become the number-one killer of young people between the ages of 20 and 45 years of age in major metropolitan centers.
NARRATOR: And by 1992, it was the number-one killer of young men in the country as a whole.
SAAG: More than trauma, cancer, suicide.
(chanting): Typical day at the N.I.H.!
Watching people die!
NARRATOR: Frustration was boiling over, especially in communities that were hardest-hit by AIDS.
And there was growing recognition that it wasn't only gay men who were at risk.
♪ ♪ Because of the... (cameras clicking) ...the H.I.V.
virus that I have attained, uh, I will have to retire from the Lakers.
NARRATOR: NBA All-Star Earvin "Magic" Johnson put a new face on the epidemic.
CHRISTOPHER HAMLIN: No one thought Magic Johnson, not Magic Johnson.
We put our athletes on a pedestal and think, "Nothing will happen to them.
They're giants, they're heroes."
That's why I am going to be a spokesman for this H.I.V.
virus, because I want them to understand that safe sex is the way to go.
I think sometimes we think, "Well, only gay people can get it, only... Well, it's not going to happen to me."
And here I am saying that it can happen to anybody.
HAMLIN: So, when Magic Johnson disclosed his status, it really was an earthquake event.
NARRATOR: When that earthquake rattled through Birmingham, the Reverend Chris Hamlin was pastor of the city's historic 16th Street Baptist Church.
Everything that is connected to the African American community has filtered through, for the most part, filtered through the Black church.
NARRATOR: 16th Street had been a major rallying point during the civil rights movement.
And also a target.
HAMLIN: Sunday, September 15, 1963, Klan placed sticks of dynamite underneath an exterior stairwell.
And that Sunday morning, young ladies were in the restroom area, getting ready for, for morning worship, when the bomb went off at 10:22.
NARRATOR: It was a horrifying attack that killed four girls.
But it cemented the role of the Black church as a powerful voice in the community.
HAMLIN: This is one place where information can be disseminated.
We demonstrate that we, one, are compassionate, but also that we're responsible for, for sharing information that is healthy and helpful.
I've always had friends-- two, especially-- who confided in me that they were gay, and both of them died from complications from, from AIDS.
Neither one of them chose to tell me that they were H.I.V.-infected.
But after their deaths, one of the members of our church said, "Oh, okay, as, as pastor of 16th Street, you've got to do more than what you're doing."
And kind of insisted that I do more.
And he was absolutely right.
NARRATOR: Hamlin joined the board of AIDS Alabama and began to spread the word about H.I.V.
to the greater African American community.
I don't know if I was the first, but in Birmingham, I, I probably was one of the first pastors who openly talked about H.I.V.
If you are a Christian, just live the life of a believer in Christ by demonstrating Godly love to all people!
Live by the Golden Rule: "Do unto others as you want others to do unto you."
(churchgoers murmuring in agreement) H.I.V., especially in the Black community, has always been viewed as a gay disease and presented itself primarily in the white gay community.
So we were, we were in denial: "No, this is not about us.
"This has nothing to do with us.
This is about, about them."
But then, as time went on, you began to see, you know, "Oh, this is about us, too."
(chuckling) Sir, what's going on?
NARRATOR: Eventually, Hamlin became the chaplain at the 1917 Clinic, working side by side with Mike Saag and Tommy Williams.
HAMLIN: One of the challenges in the Black community has always been, human sexuality is a taboo subject.
We do it, but we don't talk about it.
was one of those things, you had to talk about it.
NARRATOR: Those same conversations are still a challenge today.
WILLIAMS: And stigma is so present that it puts a chokehold on, like, any type of communication happening around H.I.V., and any discussion that happens around H.I.V.
and/or AIDS is going to have a negative connotation to it.
SHIRLEY SELVAGE: Hey!
(laughs): You knew I was comin'.
NARRATOR: Change is painstaking and very personal.
I want it like the bob.
Like the picture!
So before I came to Birmingham, you know, I married my little high school sweetheart and he went to the service, and came back, and we had a house built.
And I had my daughter then, and I think she was, like, seven.
And he literally didn't tell me, like, until three years, like, three years.
And when he told me, he was, like, "This is what I've been going through," and gave me this piece of paper.
NARRATOR: Shirley's husband was H.I.V.-positive.
SELVAGE (exhales): It took me, like, three months to really share, because I, my, the way I reacted to it, and, you know, tried to overdose, and do, tried to have... You know, suicidal thoughts of doing things.
And finally, when I told my grandmother, she was, like, "Well, Magic Johnson has it.
Girl, you better go and live your life."
I'm, like, "You don't even understand, when this get out."
And then she end up... You know how grannies do, honey.
They don't think nothing wrong with nothing.
So she end up telling family members, and then that's how it just got all out in the community.
And so I just totally, like, isolated myself from that community, until, up until I moved to Birmingham.
Are we done?
I think we're done.
You should go and have a look-see.
Ooh, I like this.
WILLIAMS: Chaka Khan, let me rock you, let me rock you, Chaka Khan.
(Selvage laughing) That's all I want to do.
The thought process in a lot of people is, "Oh, he's H.I.V.-positive.
How did he get it?"
Or, "She's H.I.V.-positive.
What did she do to get it?"
And people who are living with H.I.V., one of the things they fear most is judgment, stigma, and rejection.
♪ ♪ NARRATOR: Back in the early '90s, as Hamlin was starting tough conversations about H.I.V.
with his congregation, the scientific community was racing the clock, testing new ideas to stem the tide of disease.
REPORTER: ...cancer-fighting drug interferon... NARRATOR: Doctors, scientists, and pharmaceutical companies were experimenting with new drugs and trying them in combinations.
GANDHI: The biggest lesson was that H.I.V.
is very clever and can evade, uh, AZT or a single agent.
And so it really taught us that we have to kind of hit H.I.V.
on multiple points, multiple parts of it, of its replication pathway to get it to stop replicating.
And so it made us really start thinking that two drugs, and even three drugs, were the most important way to really hem H.I.V.
in on all sides.
NARRATOR: Dozens of drugs and combinations were tried, including an entirely new class of medication called protease inhibitors.
They worked on the virus after it had incorporated its genetic material into the CD4 cells.
At that point, the CD4 cells begin producing long strings of H.I.V.
proteins... ♪ ♪ ...which get snipped into the building blocks of new virus particles by an enzyme called protease.
Protease inhibitors block the molecular scissors and stop the virus from replicating.
The protease inhibitors were tested in combination with other drugs.
And one three-drug combination stood out.
It was about to change the trajectory of H.I.V.
REPORTER: The AIDS epidemic could well be at a turning point.
REPORTER: The three-drug combination... REPORTER: ...can reduce the AIDS death rate dramatically.
NARRATOR: The shock wave rang out from the 1996 International AIDS Conference in Vancouver.
PETER PIOT: The new combinations of antiretroviral drugs are holding out new hope.
And I just almost dropped the pencil and said, "Oh, my goodness."
This was so striking.
NARRATOR: The headline: a combination of three drugs, two reverse transcriptase blockers and a protease inhibitor, successfully kept H.I.V.-positive patients from developing AIDS.
I knew this was special.
NARRATOR: It was the so-called triple cocktail.
One drug on its own couldn't keep up with H.I.V.
But the cocktail, with its multiple drugs targeting different parts of the replication cycle, beat back the virus before it could evolve resistance.
So in patients who started using it, and we saw these dramatic drops in virus, and that was the beginning of, at least for us, using triple drug therapy.
I sort of watched at San Francisco General, the beginning of the year, 40% of our patients in the inpatient setting at this hospital be living with AIDS, um, really sick, really didn't have those antiretroviral therapies, and then I just watched, over the second half of my residency, people rise from the dead.
GANDHI: It was literally a Lazarus effect to watch these antiretroviral therapies come out.
NARRATOR: One by one, the patients recovered.
Almost immediately, annual deaths from H.I.V., steadily climbing since the early 1980s, began to plummet.
For the first time, people could truly talk about living with H.I.V.
JOHNSON: The newest drug out, which is doing great and having great success with it, it's called combination.
That's probably the reason, uh, for my good health, as well as God, just praying every night.
Thank you so much.
NARRATOR: Triple therapy was a life-saving breakthrough.
was no longer an automatic death sentence.
But it was not without its challenges.
There were some pretty significant side effects.
And oftentimes, it was a handful of pills.
It was like breakfast.
CHUNG: It was, like, six pills that you have to take in the morning, six pills you have to take in the evening, and they're, like, about this size, um, and it made me so sick.
But there wasn't any other choices.
NARRATOR: Even that changed fast.
Pharmaceutical companies continued to work on new drugs and new formulations that were more effective, easier to take, and had fewer side effects.
Within a decade, the regimen was down to a single pill a day.
It was called Atripla, but it was three medications all in one pill-- one pill once a day, big deal.
NARRATOR: Treatments were rapidly evolving, but a vaccine remained elusive.
COHEN: For all these years, it's been, "We're gonna make a vaccine and that's gonna fix the problem."
And, and certainly it's not through lack of effort.
NARRATOR: Billions of dollars had gone into vaccine research, with dozens of clinical trials, but still no vaccine.
From 1981 to 2011, that is 30 long, long years where there was no effective biomedical prevention strategy.
There was no vaccine, there was no shot, there was no cream, there was no, um, pill.
We had condoms, we had abstinence, we had monogamy.
We had nothing in terms of biomedical prevention strategy.
Now let me get my white coat.
It's the most important thing in this.
NARRATOR: The best prevention traditionally comes from vaccines, but now, a new approach was needed.
Myron Cohen was a physician-researcher at the University of North Carolina.
I was charged and committed to prevention in the absence of a vaccine.
The idea was, let's use antivirals to stop the spread of H.I.V.
NARRATOR: The concept was simple, yet unorthodox.
It was based on the concept of the viral load, the amount of virus in a patient's body.
The higher the viral load, the more likely an infected person is to infect others.
But if doctors treat those patients earlier, and more aggressively, could they bring the viral load down low enough that the virus can't be passed on?
To what extent will we render them no longer contagious?
We're gonna call that treatment as prevention, or TASP.
NARRATOR: Treatment as prevention was just one half of the strategy.
We and others were also working on the flip side of the coin.
So if we're gonna treat the infected person to try and stop transmission, we're gonna take the uninfected person and try and develop safe and effective ways to prevent the acquisition of the virus through pre-exposure prophylaxis.
NARRATOR: Pre-exposure prophylaxis, or PrEP, was not a completely new concept.
Malaria prophylaxis has been used for years.
You basically take a medication, it's in your body, and then you get exposed to malaria and prevents you from actually getting malaria.
NARRATOR: Not a vaccine, but a short-term preventative.
So this made sense to me, to use an H.I.V.
medication to prevent H.I.V.
NARRATOR: At least, that's what they hoped.
And yet it meant giving powerful treatment drugs to people who were totally healthy.
Initially, I said, "What are we doing?
"Why are we giving medicines to people who aren't infected?
That seems kind of crazy."
ELOPRE: A lot of people were concerned that it might increase high-risk sexual behaviors.
REPORTER: Some groups are concerned using Truvada for prevention would cause more H.I.V.
It could be misinterpreted as, you can engage in any risky behavior that you want.
A catastrophe for AIDS prevention in the United States.
NARRATOR: There was also a question of basic human nature: would healthy people really take this medicine?
The skepticism was, could people take a pill every day, which was hard enough to do in the treatment world.
It's been harder to, for people to take preventative medications.
WOMAN: How're you guys doing?
NARRATOR: Despite the concerns, the trials forged ahead.
In 2000, we started then a series of trials.
NARRATOR: The separate trials, conducted in multiple countries, looked at both sets of people: those who might spread the virus and those who might get infected.
For H.I.V.-positive patients, could antiviral medication render them safe as partners, no longer able to spread the virus?
And could the same antiviral drugs shield healthy people from infection?
It was a brand-new approach to prevention.
The big PrEP study was called iPrEx.
GANDHI: Oh, there was a lot of pressure riding on the study of iPrEx.
Everyone in H.I.V.
was waiting for it.
This was the first time that there would be a pill where you could prevent getting H.I.V.
I was waiting with bated breath.
NARRATOR: The answer came in the closing days of 2010.
♪ ♪ GANDHI: When I saw the results, I was elated, I was amazed.
I was so excited.
NARRATOR: In iPrEx, PrEP cut the risk of new infection by more than 70% for people who stuck to the regimen.
Further studies show PrEP cuts the risk of H.I.V.
infection from having sex by 99%, and at least 74% for people who inject drugs.
PrEP relies on the same type of drugs as are used for treatment.
Taken as a preventative medication, it creates a defensive shield.
GANDHI: And the H.I.V.
comes into your body, but that medication comes and attacks it and prevents it from essentially infecting your cells.
NARRATOR: That still left the TASP trial, Cohen's landmark study of treatment as prevention, the second part of the strategy.
Their data were still being analyzed at the National Institutes of Health.
It was a closely kept secret.
COHEN: I got a call from the N.I.H.
saying, "Can you come over to the N.I.H.?"
So we all drove over to the N.I.H.
They're in a room with a large group of people, including the leader, Dr. Dieffenbach.
And then after a few minutes of, of cajoling, he kind of...
There was a huge stack of papers and he threw up this stack of papers in the air and said, "This is a home run."
NARRATOR: Treatment as Prevention worked.
We reported that we stopped the transmission of H.I.V.
by more than 96%.
NARRATOR: An H.I.V.-positive person whose treatment brings the viral load so low as to be undetectable will not transmit the virus.
DAVID: Me being undetectable means be, being able to live again, actually live a normal life, and not be scared.
♪ ♪ NARRATOR: With TASP, for infected patients, undetectable equals untransmissible.
It's now a federal education campaign.
U equals U.
And you know what that means: that undetectable is untransmissible.
(applauding) GANDHI: It's been huge, because for science, it really shows that a preventative medication can be taken every day to prevent infection.
NARRATOR: Together, U equals U and PrEP showed a path forward.
For the first time, people dared to imagine the end of the epidemic.
Overnight, the world changed.
(whistles blowing, crowd cheering) NARRATOR: Over the previous two decades, new H.I.V.
infections in the U.S. averaged nearly 60,000 a year.
As PrEP and U equals U came into widespread use, that number fell nearly by half, while deaths have fallen nearly a third.
GANDHI: It really helps with relationships, helps with partnerships.
Watching the progression and how many advances we've had in H.I.V.
has been thrilling.
NARRATOR: 30 years after H.I.V.
was discovered, doctors finally had both treatment and prevention tools at their disposal.
That still left the challenge of getting them to all the patients who would need them, the so-called last mile, that could truly end the epidemic.
San Francisco, with its large LGBTQ community and long history of fighting the disease, is trying to lead the way.
In 2013, it set a goal of being the first city in the world to eliminate H.I.V.
The plan focuses on groups at highest risk, people on the edge of society.
MIGUEL IBARRA: Which way should we go?
NARRATOR: Miguel Ibarra leads an outreach team for the San Francisco Community Health Center, located in the Tenderloin.
Have they come and told y'all about the linkage center yet?
NARRATOR: The center works to bring H.I.V.
care, along with other healthcare, to the most vulnerable.
IBARRA: You might be experiencing homelessness.
You might be actively using.
You can show up here to SF Community Health, and you can meet with providers who have walked in your shoes and who have come out on the other side.
NARRATOR: With any disease, the last mile is always the hardest.
The hardest cases, the people hardest to reach.
You want a snack?
Here you go.
NARRATOR: But by focusing on this vulnerable population and making antiviral medication available for free-- that's PrEP and U equals U-- the city was down to 131 new cases in 2020, a 64% drop since the city set its goal of ending the epidemic.
Would you like a rapid COVID test to have?
NARRATOR: But with COVID came new challenges.
Prior to the COVID pandemic, we were actually doing really well.
And I was seeing very few barriers to, hopefully by 2030, getting to the end of the epidemic in San Francisco.
Essentially, our homeless population increased, and so did substance use.
And substance use is a really big barrier to taking medications every day or to stay virologically suppressed.
NARRATOR: Cecilia Chung knows the challenges firsthand.
In the 1990s, she ended up on the streets, using drugs, before managing to pull her life back together.
Oh, my God, that was 30 years ago.
CHUNG: If somebody is homeless, and they're very transient, they move from place to place and have to set up camps, um, or live in a shelter, where are they going to put the medications?
A regular schedule is necessary in terms of scheduling for regular doctor's visits and also blood work.
And not to mention, you know, taking medications on a daily basis.
NARRATOR: Trans:Thrive, part of the San Francisco Community Health Center, is tackling some of those exact last-mile problems.
(talking in background) ROYCE LIN: So my name is Dr. Royce Lin, and, uh, I'm a physician with the San Francisco Department of Public Health.
The work that we do here is comprehensive.
We have psychosocial services, including onsite, uh, psychiatry, medical social work.
Many of our clients here face challenges from multiple levels, and H.I.V.
oftentimes is pretty low on the priority list, compared to things like mental health, housing, where am I going to sleep tonight?
JOHANNA BROWN: My name is Johanna Brown.
I came to see my doctor, Dr. Royce Lin, to get some lab works done, and to change some medication.
I see them for everything-- financially, medically, housing.
LIN: How do we help people who have lost hope and lost the motivation?
And the work that lies ahead is the hard work of building somebody back up.
Helping people to find the strength and the hope to be able to continue.
NARRATOR: In Alabama, the last mile feels a lot longer.
HAMLIN: In our clinic, we're still seeing 12 to 14 new patients every week-- every week.
So again, that kind of gives the picture that this virus is still being transmitted.
Um, so there's a lot of work for us to still do.
NARRATOR: The Southeast is the region of the United States where H.I.V.
has the largest footprint.
ELOPRE: We make up about 50% of H.I.V.
(chuckling): About a third of the U.S. population.
So there's a disparity there.
NARRATOR: Just as it is in San Francisco, a big part of the problem is poverty.
WILLIAMS: Poor healthcare, access to resources, low education, communication.
Con-- like, it's all of that.
If you're hungry, you're not thinking about your overall wellness from a health standpoint.
HAMLIN: We have a PrEP clinic at our clinic.
It's, it's a wonderful tool.
The, the good news is, if you take it and take it properly, you would not contract H.I.V.
Unfortunately, uh, if you don't have insurance... (chuckling) ...you know, getting PrEP drugs are, are near almost impossible.
All right, thank you.
NARRATOR: While many states extend at least some health insurance to all residents, Alabama, like most states across the South, does not.
Ten percent of the state population has no health insurance at all.
Without insurance, the cost of PrEP is nearly $2,000 a month.
An insurmountable obstacle for almost anyone who comes to see Tommy.
(chuckling): Like, it's absurd.
They say, "I want to get in care, but I can't afford the medication."
NARRATOR: Through a variety of programs, the federal government offers subsidies to offset the cost of PrEP for those who qualify, just as it heavily subsidizes H.I.V.
♪ ♪ And yet, nationwide, just one in four people who would benefit from PrEP has a prescription.
In Alabama, the figure is even lower.
WILLIAMS: I don't know a lot of Black people in the LGBTQ-plus community that are on PrEP at all.
NARRATOR: The reasons are complex, but money is not the only factor.
Many patients, especially younger ones, are unaware that PrEP is even an option.
I believe one of the many reasons that the kids aren't accessing PrEP is because either they don't-- believe it or not-- know about it, they... And if they know about it, they don't really understand it.
Or they are not accurately identifying their level of risk.
NARRATOR: It all puts a premium on patient education and community outreach.
Thank you all for coming out tonight.
ELOPRE: There's been a huge push to respectfully partner with community-based organizations, because now there's a recognition that you're just not going to have the impact if you're only doing things from an ivory tower or from a research institution, where we haven't really gained that trust.
Any of you would like to share with me what your superpower is?
WOMAN: I'm a mother.
I'm a father.
I'm a friend.
I'm able to just stand firm in my truth.
So when you have a difficult situation, sometimes you cannot control that situation.
But you can control how you respond to it.
Thanks for being amazing.
All of y'all are just... extraordinary.
(group cheers and applauds) ♪ ♪ NARRATOR: Throughout the long battle against H.I.V., the goal has been to remove scientific and societal barriers to make treatment easier.
How are ya?
NARRATOR: And the next advance, a new formulation of PrEP, is trying to do both.
Some of the insurance issues around... NARRATOR: Instead of a daily pill to protect against infection, the new iteration is an extended-release injection that lasts for two months.
Do you want to remain on the injectable PrEP or go back to the daily pill?
(chuckling): "I won't forget to take the pill."
I think I've forgotten to take the pill once or twice over the weekend.
And now it's, like, "Okay, I know I've got my shot, I'm good for my shot until my next appointment," so I don't forget to take the pill.
NARRATOR: Every two months is just a first step towards protection that patients barely have to think about.
GANDHI: I think the next goal would be an implant that actually you put under the skin and it protects you for a full year.
NARRATOR: Coming full circle, variations of the drug combinations already approved for prevention are now being tested as a longer-acting treatment for people who are H.I.V.-positive.
NARRATOR: Tommy is one of the first people to get it as part of a clinical trial.
WILLIAMS: I got put in the four-week arm.
I really wish it was the eight-week.
'Cause I have to come every month.
And that can be hard for a lot of people.
How are you today?
Have a seat.
So today is gonna be your last study visit.
And we can transition you from the every-four-week injection to every-two-month injection.
(laughing) So you will go from 12 a year to six a year.
(laughing): Why am I about to cry?
I am so excited!
(laughing): You know I've been wanting that two, that two-month for the longest.
I know, I know, and so... Oh, my God.
Bye-bye 30-day injections!
I don't wanna do it, I don't wanna do it right now, 'cause I don't wanna be... Oh, wow.
All right, I'll see you-- I'll see you.
♪ ♪ NARRATOR: The last mile, like the rest of the victories against H.I.V., will come one hard-earned step at a time.
Which won't make crossing that finish line any less remarkable.
I'm really glad to see you.
SAAG: And it really is pretty miraculous how we converted H.I.V.
from an almost-certain death sentence into something that I think we can call a chronic manageable condition.
HAMLIN: When I first went to the clinic, we had angel wings report.
When a patient died, we would send out an email.
And initially there was, like, two or three emails every day of patients dying.
This week, we have not gotten one angel wing email.
NARRATOR: Healthcare workers will continue to treat... ♪ ♪ ...and scientists will continue to innovate.
The toolkit, impressive as it is, still needs to grow.
Especially as we tackle H.I.V.
in the rest of the world.
Longer-term PrEP options are being tested, as are new mRNA vaccines, building on COVID-19 advances, that sprang directly from pioneering research into H.I.V.
was the NASA of COVID.
The COVID vaccine came out of the Vaccine Research Center, which was created to make an H.I.V.
The treatments that we use for treating COVID are really spun off completely from H.I.V.
Paxlovid is a protease inhibitor.
GANDHI: So ten years ago, if you had told me that prevention could have dropped infections by half without a vaccine, I would not have believed it.
That was also miraculous.
MASCOLA: I think PrEP can get us to zero.
It's just a matter of the resources needed to hold us there.
ELOPRE: We have a medication that you can take that almost 100% prevents you from getting H.I.V.
if you're exposed.
So 100%, if we were able to improve access, I think we could end the epidemic.
HAMLIN: Not one institution can be isolated and say, "I'm not affected by H.I.V.," or, "I'm not affected by healthcare issues," because all of us are.
GANDHI: I am very hopeful now that we have the tools to see the end of all new H.I.V.
infections, the end of AIDS deaths, and the end of AIDS stigma.
That is what I want to see in my lifetime and I absolutely know I can.
WILLIAMS: We have the tools to stop it.
Let's do it.
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Or call 1-800-PLAY-PBS.
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