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Interview

The Future of HIV Prevention, Treatment and Care
An Interview With Mark Harrington

By Terri Wilder

June 23, 2014

Mark Harrington

Mark Harrington

TheBodyPRO.com recently interviewed longtime activist Mark Harrington, the executive director of Treatment Action Group. Harrington talks about the ramifications of the PARTNER study results, as well as what to expect from HIV treatment and care in the next five years.

How is HIV prevention changing today?

One of the really interesting things about the renewed discussion and debate about prevention in the gay community is that a lot of people are explicitly beginning to say one of the goals of ending the epidemic is to be able to have condomless sex without being worried about HIV transmission. And there are some people who can do that today, right? If you're in a seroconcordant relationship and you both got tested yesterday, and you've been totally faithful since then, you probably could have sex without a condom today. And if you're in a serodiscordant relationship and one person's got an undetectable viral load, or their partner's on PrEP [pre-exposure prophylaxis], or both, you can probably have condomless sex without risk of transmission.

Even from the PARTNER study recently -- even just one partner being virally suppressed, and the other being negative, it seems like the rate of transmission was low, was very low, in the first two years of the study. It was so low that nobody got infected, which implies that a controlled viral load is pretty safe, safer than what we used to call unsafe sex. And so we need to rebrand; we need to rethink safer sex. We can't just keep on using the same old messages from the '80s and '90s, because they're obviously not working.

We need to add new tools to the arsenal of sexual health. That includes PEP [post-exposure prophylaxis], PrEP and fourth-generation testing, with more frequent testing if you're in a high-risk group. Most people don't know about these new tools and how to use them. It's been very exciting to see in ACT UP a real hunger and awareness, interest in the emerging new science around testing incidence, transmission and epidemiology. If there were more places where those conversations were going on, I think we could have a new generation of activism to really stop the epidemic.

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In terms of the PARTNER study, what should medical providers be saying to their clients?

They should say it's really early days yet, and the sample size is small, and the error bars are large. So far, there have been no transmissions observed. But if we run it out longer and with enough people, eventually there's going to be some.

How much longer, and how many more people?

Well, you can see what Jens Lundgren said about the confidence interval. He was very clear that it's really early days in the study. And the study is not saying it's 100 percent fail-safe; they were very careful about that.

On the other hand, I think it's undoubtedly good news, for that number of people followed for that length of time, that nobody's been infected. That would appear to concord with the 052 study, where there was really zero infections after treatment started. The one infection that happened in the treatment arm was already underway at the enrollment period of the study, which, remember, nobody could believe it when it came out.

What it also shows you, which is unlike the PrEP studies, the adherence to treatment in 052 was incredibly high, or there would have been more infections. There were no infections in the treatment group, except for that one at baseline. In most of the PrEP studies, adherence was all over the map. That's one of the valid issues that people had about the PrEP studies, is that adherence is all over the map. But on the other hand, now that we know PrEP works, adherence might be better, at least, in some groups. Theoretically, you could do tests for adherence with blood levels.

Furthermore, in a few years, when tenofovir [Viread] comes off patent, you'll be able to get PrEP for about 200 bucks a year.

When's that going to happen?

In about 2017. And the long-acting injectables will come around. There will be no adherence for them, unless you just don't get your shot.

So the outlook for chemoprophylaxis is just going to get better. There are going to be more options available for more delivery mechanisms. Even on some of the lists that I've been on, you can see the discussion is shifting from a discussion about condom Nazis or people who are condemning barebacking to much more of a discussion about people saying, "Well, I've started it." "I'm starting it." "I'm thinking of starting it." "Why did my doctor send me to a specialist just to get a prescription?"

People are at least willing to say that they are considering doing it. I think that's a really good sign. People were absolutely desperate for stuff. They were even willing to do stuff that didn't work for a long time, because there was nothing that worked or because there was nothing that they knew worked. And then, as the years went on, some of us asked for higher standards of data. Because some stuff worked for a little bit, but it didn't work for very long. And we wanted it to work longer.

We need to have standards for data and high-quality data in prevention, just like we do in treatment. People shouldn't be still putting crap in our bodies, and people should be able to use any tool that can help them not become HIV infected, whether that means more frequent testing, chemoprophylaxis, barrier methods, legal clean needles or [circumcision].

Let's talk about care and treatment for the person with HIV. Anything exciting that you think is going to be coming down within the next five years?

Well, I think dolutegravir [Tivicay, DTG] is very exciting. It's probably more exciting from the global standpoint, because it will enable us to have a cheaper second-line and maybe even first-line therapy than what we have now because it's going to be cheap to manufacture. It seems to be very potent. It's really the first drug that's come along that's really clearly more potent than efavirenz [Sustiva, Stocrin] and either more potent or equipotent with the protease inhibitors, darunavir [Prezista] and atazanavir [Reyataz]. So we really have an integrase inhibitor that's as good, or more potent than any of our other drugs. And it's a small molecule, once daily, without a booster. It's a huge breakthrough. It also happens to treat raltegravir [Isentress]-resistant [virus].

Are we concerned about resistance?

Anytime you have an antimicrobial drug, there is going to be resistance. The only way to prevent it is to not ever give the drug out at all. So we're going to have resistance to anything.

What's interesting is that, since the advent of HAART [highly active antiretroviral therapy], the incidence of transmitted drug resistance has actually gone down, because most of the people in the '90s that were on partially suppressive therapy, they got resistant to everything they were on. After HAART, most people don't become resistant at all if they're adherent -- or they might become resistant to one thing, and then they switch. So incidence of transmitted drug resistance is under 10%. And we've had HAART for 18 years now. It was higher in '94 than it is now.

I'm not terribly worried about resistance. I'm worried about people not being able to get treatment that they need, because of price, costs or health system barriers.

There are other drugs. But we're at the point where, in HIV therapy, things are pretty good, and getting better. I think where a lot of action is going to be is in trying to figure out how to improve our game and other aspects, like in chemoprophylaxis and vaccines. We're very, very far from having a vaccine.

Do you think we're going to see a vaccine in our lifetime?

I don't know. I hope so. I think they have a better understanding of what kind of antibodies they would like to elicit. I don't think they know how to elicit them.

What about a cure?

Well, apparently, two people have been cured: one baby and one adult.

We may have a third.

I know. That's what people said last year about the Massachusetts patients. We shouldn't count that third person until the second baby goes off therapy. All we know about is two cures right now: one baby, and one adult. Neither one has been confirmed with another case. At this point, they are exalted and exciting medical anecdotes. We don't know how to repeat them. We haven't been able to reproduce what happens in them yet. So there's nothing that's scalable about it. We can't even do it in a second bone marrow transplant patient yet. We might have a second baby, or we might not. But we won't even know for a long time, because I think they're going to wait until that baby's been on therapy at least two years, or something. And I can't remember how old the baby is.

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I think the baby is 9 months, from California.

We might as well not talk about it being cured until we find out when it goes off therapy. We have no idea. We don't know how to measure the reservoir. And the only way to find out is by taking the poor kid off therapy. It's not worth the risk until they're probably at least 2 years old.

What was the one thing at CROI 2014 that you were excited about?

The use of molecular phylogeny to interrupt ongoing chains of active HIV transmission among MSM [men who have sex with men] in San Diego, as presented by Susan Little from UCSD [University of California - San Diego], using the pol gene sequences and showing how they were assessing people's risk. Really, their risk had more to do with how many people they were connected to in their network than safety per act. And the people who are more connected in networks are more in a situation to be part of a transmission chain.

What she said, in answer to a question, was that they have data that treating people early, like within 12 weeks of infection, within those clusters could break ongoing chains of transmission. Now, she said it, but she didn't show data to show it. We assume it's an ongoing project that is either in submission or that they're waiting for more data.

What she did show was very beautiful molecular epidemiology using those data. It solicited some interesting discussions about community participation in prevention science. Because those individuals in the study have to consent. Now the state has our pol gene, for anyone that's been diagnosed. But Susan is getting their pol gene; and she's got data, I guess, before the state has it, or is outside of the state surveillance. Because she said their identifiers are being protected by a 13-key algorithm -- which means that nobody, "not even the NSA [National Security Agency]" can crack their ID. Now, of course, once it goes up to the state, anyone with the password to the state database can get it.

So they're concerned about the issues of community consent. They're addressing them in a prospective way. I think there's an obvious concern about if you document the relatedness of various strains of HIV, that if there's a criminalization law in your jurisdiction, those data could be used in a very, very harmful way.

But so far as we know, that hasn't been the case with these datasets up to now. And we need to make sure they're protected. But we do have the molecular tools to start interrupted ongoing chains of transmission if we can get community buy-in and willingness.

Really, it's almost like thinking about partner notification and contact tracing before you get infected, instead of after. Like, what if we did the New York Chemoprophylaxis Registry, where everyone who got PEP or PrEP was in a registry? And then, by definition, they're in an intervention cohort where you could start getting data on their networks, and then could potentially reach out to people in their network and say, "Hey, do you want to join this cohort? It's a chemoprophylaxis cohort. It's designed to help people stay negative."

And we could build on that -- just the way we have transmission networks -- to have non-transmission networks. Wouldn't that be cool? To me, that was the most exciting paper of the meeting.

What advice do you have for a young activist who's just starting out?

People ask me that kind of thing all the time. People have to find their own mission in life, their own issue, their own target, their own strategy and their own way of doing it. The one thing that older activists can do and more experienced activists can do is we can help; we can answer questions. We can help people learn. We can talk about our experiences. We can mentor people.

But you can't really mentor somebody if they don't want to be mentored. And so I think, really, it's a matter of, where are they coming from, and what do they want to do? What are the issues that really are most meaningful to them?

It's really not for me to say what a person should do with their life. This epidemic touches on almost everything that's unjust about our world. And yet, at the same time, in this one space, humanity has made more progress and shown more solidarity with some of our most excluded and despised brothers and sisters than we have in many other cases. And so, out of great suffering, some great human work has been done.

And we're far from finished, so there's plenty of work for everyone. I think we should all try to figure out how to end the epidemic as quickly as possible. But there's not one way to do it.

This transcript has been lightly edited for clarity. Due to poor audio quality, this episode of HIV Management in Depth is transcript only.


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