Viremic – Cases in HIV

Announcer:
Welcome to Viremic–Cases in HIV, hosted by Dr. Eileen Scully and Dr. Christopher Hoffmann, both HIV specialists at Johns Hopkins, who explore quandaries in adult HIV care. Each case discussion includes medical history and diagnoses, challenges in care and treatment, and key evidence and guidelines that inform clinical decision making.

Cases are presented as a composite from the hosts’ clinical practice, with all identifying details removed to protect the privacy of patients. Case discussions are for informational purposes only and not offered as medical or clinical practice advice for patients or clinicians. Any mention of specific medications or commercially available products is a description of use only, not an endorsement.

Dr. Eileen Scully:
Welcome to Viremic, a podcast where we discuss all things HIV. I’m Dr. Eileen Scully and I’m coming to you from Johns Hopkins here in Baltimore, where I’m joined by my friend and colleague, Dr. Chris Hoffmann. Before we begin, a reminder that if you like this episode, please share it with a colleague and follow us wherever you listen to podcasts. We’d also love to hear what you think, so please leave a comment or send us an email at viremicpodcast@JH.edu, and feel free to leave suggestions for future topics you’d like us to discuss.

Hi Chris, happy fall. Good to be with you today.

Dr. Chris Hoffmann:
Great to be with you also.

Eileen:
Today I’m going to start with an actual real-life question that a patient asked me this week, which was, to paraphrase, “Is this every-six-month injection treatment real or is that fake news?” So, I’ll start by asking you, Chris, is this a question that you’ve had yet in your practice?

Chris:
It is a very common question. The two big questions I get regularly asked are, “How close are we to a cure?” and “Can I get the every-six-month treatment?”

Eileen:
That is increasingly common with my patients as well.

Chris:
I think there are a number of reasons that patients ask that. Sometimes I explore a little bit more and then discuss where the science is. But I think it really highlights, partly, the stigma that they feel. And even if they don’t verbalize that, cure obviously takes HIV totally off the table if it’s a true cure of HIV, and even the six-month injection reduces their need to think about HIV and feel the stigma, internalized or enacted stigma, regarding HIV.

Eileen:
Chris, those are excellent points, and I think it’s also a really important perspective check. Because to me if, for example, you’re on every two-month injections of CAB [cabotegravir]/rilpivirine, you actually have to go to the clinic more frequently than if you were taking a daily oral pill. From my perspective as a provider, I might think that that was more burdensome. However, as someone pointed out to me, that means that instead of thinking about your HIV every single day when you take a pill, you actually only have to think about it six times a year when you go and get your injection, which is like a dramatic and radical transformation. That’s not how every patient feels about it, but I think you’re highlighting a really important thing about the injectable therapies that is important to explore with a patient who’s considering having that as part of their regimen.

But to your point, Chris, that’s exactly what I answered this patient. There is a once every six-month [treatment], but we don’t actually have an available regimen for which that’s the only treatment that you get. So, you can use lenacapavir, but typically it’s used in combination with other agents. However, this leaves out the recent results that you presented a few weeks ago on the podcast with Dr. Joel Gallant summarizing results of a trial that was presented at the AIDS 2026 meeting.

This trial looked at twice-yearly administration of lenacapavir, so every six months, together with 2 broadly neutralizing antibodies [bNAbs], which are nicknamed “TAB” [teropavimab] and “ZAB” [zinlirvimab], and I will not be trying to say the full name. The TAB is an antibody to the CD4-binding site, the ZAB is an antibody to the V3 glycan loop. These have been modified to maintain their levels in the body for a long period of time, and so they can be used every six months. What they showed at AIDS 2026 was follow-up to earlier results; they showed the 104-week outcomes of this combination regimen in people who had been already suppressed on a regimen of oral antiretroviral therapy. What they saw was that it worked quite well, that there was a high level of maintenance of viral suppression, and there were only two participants who met criteria for virologic failure. Actually, one met criteria and the other had confirmed rebound and was discontinued based on investigator discretion, just a slight difference in terms of study protocol, but both of them had some viremia. Overall, very promising results for our first ever once-every-six-month treatment. However, I think there are some really important details in terms of who was included in this trial that get to the heart of some of the questions and concerns about broadly neutralizing antibodies.

Chris:
I think [it was] really an exciting trial—exciting that there was something to pair with lenacapavir for once every six-month dosing. And as you pointed out, this was the two-year results, which means that participants who received the investigational agent throughout the entire trial had four doses of HIV medications compared to over 700 daily tablets for those who were in the care-as-usual arm, which just thinking about it, is to me just such an amazing difference and for many people could be such a change in their life, lifestyle, and conception around HIV.

However, I’m not sure that this is going to be the final way that we get to an every-six-month treatment. In terms of the study, there were approximately 240 individuals who were screened for eligibility, with an important screening simply whether their HIV would be susceptible to the broadly neutralizing antibodies or bNAbs. Of those 240 participants, about 40 of them had an assay failure, so the assay that was being used was simply unable to determine whether they had susceptibility or not to those bNAbs. Of the remaining approximately 200, half of those individuals were not susceptible.

Although, clearly, they had not received bNAbs in the past, just naturally the HIV they were living with was resistant to the two bNAbs being used in this study, which left less than half of the original potential participants who were being screened able to be enrolled in the trial. So, of those 241, there were only 99 who were actually identified to be susceptible to both of those broadly neutral antibodies, and then of those, only about eighty-four who were actually enrolled in the trial and randomized to the two arms.

Eileen:
That’s a really sobering set of numbers to go from 241 to ultimately those who were randomized and dosed being only 80, and I think it highlights one of the key concerns about broadly neutralizing antibodies. I share your question about whether or not bNAbs are the way we’re going to get to a sustainable every-six-month therapeutic, but I will also say that it seems to be the every-six-month therapeutic that is closest to actually being available. So, for this episode today, I thought maybe we could take a few minutes to talk about broadly neutralizing antibodies themselves and what kinds of questions we have about them and how they might fit into the therapeutic landscape.

Chris:
You are far more knowledgeable about bNAbs than I am, so just starting with a very basic question, Eileen, perhaps you can just describe what bNAbs are and perhaps how they’re developed in 2026.

Eileen:
Great, happy to talk about it. So, neutralizing antibodies are little components generated by the immune system that bind to infectious particles, and once they’re bound to an infectious particle, they prevent that, in this case HIV, virus from infecting a cell. Because essentially what they do is they cover the parts of the virus that interact with the CD4 cell.

If it’s decorated with these antibodies, the virus no longer has room to actually fit its envelope down onto the CD4 cell, and so it doesn’t get in. This was highlighted in lots of public information about SARS-CoV-2, and you know that picture of the gray virus, the little maroon spikes, and then the antibodies would bind to those maroon spikes so it’s exactly that principle. The antibody binds to the outside of the virus, and it prevents it from getting in.

Now when the body first sees HIV, it generates a lot of antibodies to all different parts of the virus, but only the ones that actually bind over the binding sites, or the sites of contact between the virus and the host cell, actually help. A lot of the antibodies that we make initially when we see HIV don’t really do that much to prevent infection. Neutralizing antibodies are those specific ones that when they bind the virus they prevent that interaction and don’t allow the virus to infect the cell. So, they’re essentially neutralized—an enemy that is neutralized. Does that make sense?

Chris:
Yes, it does, and I know there’s been interest in broadly neutralizing antibodies for many years for a variety of viral conditions, specifically HIV. But early on, it seemed like there were a lot of challenges to getting broadly neutralizing antibodies that were effective. What has changed in terms of our ability to better either target or isolate optimal antibodies?

Eileen:
Those are great questions, Chris. I’m going to make one more definitional point and then let’s talk about that. A neutralizing antibody is one that neutralizes the virus. A broadly neutralizing antibody is one that can do that to a lot of different strains of HIV. That grading system of becoming a broadly neutralizing antibody, getting that exciting title, is based on a number of different isolates representing viruses from diverse parts of the globe. Some antibodies that bind to HIV and prevent infection will only do that to certain viruses that are what we would call fairly easy to neutralize—there’s three different tiers—and some can actually neutralize many, many different kinds of HIV. The challenge with HIV is similar to the challenge that we see in resistance. HIV has this error-prone reverse transcriptase and can rapidly make changes in itself, and so once the virus evolves a little, it can sometimes escape from one of these antibodies and then it no longer works. Finding a broadly neutralizing antibody means finding one that will work in viruses that are found in people in sub-Saharan Africa, in Baltimore, in Paris, in all these different sites in which there are different pressures on the virus. And so that’s been a major challenge.

The other challenge is that there are just features of the antigens, the things on HIV that are recognized by the immune system, that make it difficult to develop an effective antibody. The HIV is decorated by glycans, which are these sugar-derived moieties, that obscure some of the parts of HIV and make it more difficult to find the perfect antibody to bind and neutralize this.

So, your question was what’s changed over time, and I would say that one of the features that’s changed over time is our ability to isolate these antibodies, because the source of these broadly neutralizing antibodies is from people living with HIV or their B cells. So, when people are living with HIV, over time the immune system keeps evolving and trying new antibodies, and many people will develop antibodies specifically to their own virus. A small subset of them will actually be neutralizing, and an even smaller subset of those would neutralize other people’s viruses as well and would start to get to this broadly neutralizing status.

Over the last 15 to 20 years, using a variety of techniques in the lab, several investigators have been able to isolate different antibodies that can neutralize many tiers of HIV from individuals living with HIV, and then they’ve been able to isolate that specific antibody and make lots of it. So, I would say that one of the things that’s changed is just simply the immunology technology to allow us to identify these very rare antibodies that have existed probably for a very long time within people living with HIV.

Chris:
For those who remember early in the COVID epidemic, we had a number of bNAbs that were used for either prevention or treatment of pre-Omicron virus, such as sotrovimab or bamlanivimab. Is the approach to developing these agents similar between COVID and HIV?

Eileen:
What a great question, Chris. I think that’s an excellent example of how the infrastructure of HIV research has been mobilized in other settings, including Zika and COVID, to really rapidly advance therapeutics, and how when we think about what the importance is of research in HIV, we can think not only of the results for HIV, but also for other infectious pathogens, which would otherwise not have had any kind of research infrastructure. But yes, a lot of these same techniques can be used to identify the antibodies and then for the manufacture. In order for an antibody to be a therapeutic, a couple other things have to be done to it. If I just administer an antibody, it has a relatively short half-life, so it’s gone fairly soon. So, there are certain modifications you can make to the stem part of the antibody that make it last longer and make it more effective as a sort of pharmaceutical agent as opposed to one that is gone almost immediately.

There are also important things to consider for how that antibody triggers the immune system. There are modifications you can make to make sure it either is or is not recognized by the immune system, and then there are ways to try to make sure that it does not provoke a lot of immune reaction itself, so that it doesn’t trigger the immune system to start to neutralize the antibody that you’re putting in with repeated administrations. The infrastructure to identify and then to optimize and then to manufacture broadly neutralizing antibodies that has been developing in the HIV field has clearly benefited [research in] other infectious pathogens, including as you mentioned, COVID.

Chris:
So, I’m just trying to wrap my head around the place for a bNAb versus a molecule product such as lenacapavir. Perhaps I have a bit of a bias towards drugs versus antibodies, but it seems like if we had [an] every-six-month molecule that could be paired with lenacapavir, that may have advantages versus similar dosing regimens for monoclonal antibodies.

Which gets me to another question, which is about getting the host to produce those antibodies either through some sort of mRNA process or other viral vector or vaccine that then could create a longer-term host production of that bNAb. Is that also something that is being worked on and realistic to consider in the future?

Eileen:
Those are really important questions, and the tractability of this as a long-term therapeutic is definitely a very open one. You’re correct that it would be much better if we could just give you a vaccine that would induce a broadly neutralizing antibody, such that you could boost it later, but you would just have your own cellular factories making this antibody that could provide you protection. That’s in fact what vaccines do.

There have been, you know, now many decades of research in HIV trying to develop those, and they’ve been very challenging. This is because the broadly neutralizing antibodies that have been identified to date have what is described as extensive mutation. All antibodies start from point A, but they are educated and matured once they bind to an antigen. Multiple mutations are introduced into the B-cell receptor that becomes the antibody that allows the development of an antibody that is very finely tuned to the pathogen. For HIV, this appears to require multiple rounds of mutation. So, the first time you try to mutate to recognize HIV better, you’re not quite neutralizing. The second time you get some neutralization activity, but it has to go through multiple cycles of this in order to develop this somewhat magical, broadly neutralizing antibody capability. No approach of just giving a single dose of vaccine or even multiple doses of a vaccine has been sufficient to drive that continued education. In natural infection, where people develop these neutralizing antibodies over time, they have continuous exposure to the HIV antigens for years, so that allows this continued mutational development and education that leads to ultimately this really well-suited antibody. There’s no real way that antibodies are going to be developed from just a single vaccination or the same antigen spread out over months or years.

Current strategies in the vaccine field have decided to take a different approach, so now there’s at least one strategy where they’re going to start with one immunogen, one antigen, and then the next vaccine will be slightly different, and then the next vaccine will be slightly different. And the belief is that it can sort of lead the maturation process towards this broadly neutralizing antibody, and this research into how the bNAbs were originally generated in people living with HIV is what’s informed this new approach, and we can be hopeful that over time this will be successful.

You mentioned a few other possibilities, and those are other ways of getting the body to produce this particular antibody. In terms of mRNA platforms, the classic mRNA platform for a vaccine includes the antigen, not the antibody, because it’s much smaller. So, it would be hard to administer a vaccine that would just allow you to produce the antibody. The other thing you mentioned, vectored immunoprophylaxis, so this is where you use an adenoviral vector or other vector to insert into, typically, muscle cells a virus that then over time produces the antibody of interest. So, you turn part of your body into a little factory that’s making this antibody that you need. This has been shown to work in some mouse models and has been developed but has reached some points of real challenge in actually getting to a human therapeutic. So, both of those things are being explored but [are] not quite ready for prime time. So, to summarize, broadly neutralizing antibodies in humans take probably years to develop. They also require this multiple education approach. Thus far we’ve not been able to elicit anything close to them with standard vaccines, and there’s some new very-engineered vaccine approaches that are trying to move that education along. In the background, the possibility of maybe a vectored immunoprophylaxis, where you turn some of the muscle cells into a factory for this antibody, is something that’s been explored.

Chris:
So, I often have patients express interest in participating in clinical trials, and I certainly encourage them. That’s the only way we can expand our knowledge and understand which of our hypotheses are true even with currently used treatments—whether or not they’re actually working. And one of the hesitations I have, not with any of the trials my patients have participated in but is with trials that involve an analytical treatment interruption [ATI]. I know that some bNAb trials have included that. Perhaps you can explain a little bit more why or what can be answered with bNAb research and [an] analytical treatment interruption.

Eileen:
Chris, this is a central challenge in the cure field because ultimately the only way to truly know if your intervention has been successful is to demonstrate that you have antiretroviral-free, sustained remission from HIV viremia, and the only way to demonstrate that is to stop your antiretrovirals. So bNAbs are, as you mentioned, something that’s been deployed in the cure space as well.

We’ve covered that there’s this new treatment trial, which shows the possibility of using this [bNAbs] in patients who are already suppressed and who are in the roughly estimated to be less than half of individuals who have testable susceptibility and are actually susceptible to both antibodies. So that’s one potential niche for these likely-to-be commercially available bNAbs, TAB and ZAB. The other areas that have been explored have been as a preventative, where you are regularly infused with the antibody, or for cure. In the cure space, one of the things that is interesting potentially about broadly neutralizing antibodies is that it’s possible that administering them may actually fundamentally increase the body’s immune system’s ability to recognize HIV just period, and this is called a vaccinal effect. So, you get the antibody, and the thought is that by binding HIV, it more efficiently leads to priming of the immune system, and maybe you get a better immune response from your own body’s system than you would have had without it. It is being combined with other interventions, including latency-reversal treatments or immune-amplifying treatments, in order to try to achieve a potential cure.

So, just to make it more practical, I’ll briefly mention the RIO trial. This was a trial that looked at two broadly neutralizing antibodies and virally suppressed participants who were on ART that was started early in the course of their HIV. Participants then interrupted ART after receiving blinded infusions and were offered a second infusion about 20 weeks later if they remained suppressed. Their primary outcome was the time to viral rebound at 20 weeks; the first of six values greater than a thousand copies, or two values greater than 100,000 copies. And what they found was that in the participants who received it [a bNAb], 75% did not have viral rebound at 20 weeks versus 11% of the arm that did not [receive a bNAb].

This was not maintained over time, so 25% of arm A [the bNAb arm] was still without viral rebound at 96 weeks, but it’s still a lot more than would have been predicted without an intervention. What was shown here was that receiving the antibody delays at least the time to rebound in a significant portion of people who were enrolled who were suppressed and had started treatment early in HIV, which likely increases the susceptibility.

But what you’re pointing out is that in order to show this, they had to stop antiretroviral therapy, and the criteria for virologic failure were not greater than 50 copies, they were sustained elevation in viremia. We know from other studies that having your viral load come up is not generally a great idea. You’re unlikely to have an AIDS-related complication, but there is evidence that elevated viremia is associated with increase in other morbidities, and it also leads to lots of concerns around potential transmission to partners. Analytic treatment interruptions are therefore something that is very carefully considered. We can provide a link in the show notes to a nice paper written about how to think about analytic treatment interruption and to do so with participants’ voices. But it remains something that often has to be done in order to assess whether an intervention is actually working. If that’s the goal, to stop therapy, then you have to see if you can or not. For interventions that are not likely to lead to sustained remission but we’re trying to induce an immune response or something like that, there’s a very strong argument not to do ATIs and instead to use historical controls, but that is an ongoing discussion in the field.

If you have patients who are interested in enrolling in some of these types of trials, what their partner status is, how they feel about an ATI, or an analytic treatment interruption, is an important part of that conversation and one that as a provider you can certainly assist them in thinking through.

Chris:
That’s very helpful. I wanted to get a little further explanation from you in terms of the bNAbs and some of the cure work. If I’m correct, one of the differences from [between] a bNAb [and an] antiretroviral therapy agent such as lenacapavir is that the bNAb can also help target the cell that may be harboring latent HIV based on antigens that are on the surface of the cell that then can induce an immune response to clear that cell versus an antiretroviral drug that obviously has to work just on various enzymes of the HIV.

Eileen:
That’s a great point, Chris. Yes, the antibodies don’t require the viral life cycle to be efficacious and that can be seen as a very big advantage for certain indications. When the HIV is truly latent, there are actually relatively few antigens expressed on the surface of a cell. So, for that type of intervention to be successful, likely you’d also have to turn on HIV with a latency reversal intervention of some sort, but then you could identify it by those antigens on the surface of a cell without it being released into full new cycles of replication in a way that you can’t target with just an antiretroviral drug.

That ability to recognize HIV without being dependent on the viral life cycle is an additional benefit, along with the potential for a boosting of the immune system through a vaccinal effect, although that is somewhat debated.

Chris:
You’ve nicely described bNAbs’ potential role for HIV treatment, as well as how they’ve really been an important part of cure research. Can you go into a little bit about bNAbs and prevention?

Eileen:
There have been trials of using broadly neutralizing antibodies by just infusing them in the same way they’re being used for therapeutics and for cure to see if they could then prevent new HIV acquisitions. There were the AMP (antibody-mediated prevention) trials, which were HVTN 704 and HPTN 085 and HVTN 703/HPTN 081. These trials looked at VRCO1, which is a CD4-binding-site antibody, and they had estimated that 65 to 80% of the isolates of HIV from trial sites would be sensitive to VRCO1. They did every-eight-week dosing for 20 months. So, pretty burdensome as a preventive treatment, but not daily, so that’s an upgrade there. They enrolled 4,620 participants in the U.S., Switzerland, South America, and sub-Saharan Africa, and they did offer PrEP [HIV pre-exposure prophylaxis] at the same time, but uptake was very low. For example, less than 1% of the sub-Saharan African participants had therapeutic levels of taking PrEP. What they showed was about 30% of the isolates were sensitive, so nowhere near their estimate, and among those viruses, protection efficacy was estimated at 75%, meaning if the virus was susceptible to the antibody, it did prevent infection 75% or so of the time. However, otherwise, for the vast majority of the viruses there was no effect. So, the conclusion from this initial trial was that a single antibody preventative was unlikely to be adequate, and you would need to combine broadly neutralizing antibodies into a sort of cocktail, similar to antiretroviral cocktails, in order for it to be an effective preventative treatment, and that also this type of therapeutic, with its requirement for frequent dosing and other sort of just supply chain issues, has some major scaling and feasibility considerations. So, a sobering result, one that is not an easy answer, and hopefully will give us some information if we develop better alternatives in the future.

Chris:
Yes, very important. Certainly, developing and designing clinical trials for prevention will be a challenge now, given the wonderful efficacy of lenacapavir and only every-six-month dosing.

Eileen:
I totally agree.

Chris:
Eileen, if we circle back around to your patient or many of my patients asking about [an] every-six-month treatment and a partner for lenacapavir, from what I’ve learned from you is that we certainly have this trial that showed amazing effect [in] these individuals who were in the trial and were eligible because their HIV was susceptible to the combination TAB/ZAB. bNAbs did very well, and again I’ll say what is amazing to me with only four doses of an antiviral therapy, maintained an undetectable viral load for two years compared to over seven hundred days of daily pill dosing. Yet, barriers include the resistance, having to do the assay, as well as likely high cost of these agents. So right now, even if TAB and ZAB along with lenacapavir move to a phase-three registrational trial and are approved, it seems like it would be a fairly small number of patients who would be eligible for treatment based on either their virus or their insurance coverage. What we really need is still a molecule to pair with lenacapavir.

Eileen:
Chris, I have to say I share a lot of your concerns, and one of the key things is that the participants in this trial had sustained viral suppression for over a year. Those are not the people who I most feel desperate for an every-six-month therapeutic. I will say that, you know, one benefit is that if you “lose these agents” and develop resistance, okay, we still have all of the other classes of antiretroviral therapy available to us, so it’s less of a cost than say losing the integrase inhibitor class, which is such a key part of the backbone of so many regimens. You just lose susceptibility to this particular immune-targeted treatment but still maintain all of the other range of options. So, from that perspective, it’s a good long-term agent for all the reasons you mentioned, including in particular the likely high frequency of people who won’t be susceptible to these—that’s a challenge—also, the fact that it was not studied in the people who we’d be most interested in long-term antiretroviral therapy [for], which [are] those who are unable to take oral daily pills.

I will also just put a little footnote on the fact that in this trial of 80 people, there were two individuals who had emergence of viremia. That is a much, much higher rate of viremia than one would see in a population that was adherent to their oral therapy, in which we would expect it to be truly zero. Here, these participants received their infusions, they got their lenacapavir, and yet they still developed viremia. This is a feature of injectable medications. We’ve seen it in CAB/rilpivirine at about 1%. And, I think that’s an important part of a conversation with someone if they’re embarking on a transition to this approach, especially because the people who would initially qualify would be those who are already actually doing great on oral antiretroviral therapy.

And the other consideration, which is one that you and Dr. Joel Gallant had highlighted in your summary of AIDS 2026, is that it may be a hard sell to convince an insurance company that someone who’s doing great should be shifted to a novel approach, which is likely to carry some significant costs up front. So, I agree with you. I’m not sure where this is going to fit into the therapeutic landscape at the moment, and I think that there are some ways in which a molecule, as you say a drug, is a much easier option for a longer-term therapeutic. It’s just that we don’t really have one yet.

Chris:
And research and asking questions, even if we think we know the answer, often proves us wrong and is such an important part of advancing care overall and certainly for our patients with HIV.

Eileen:
I totally agree. In the field of rheumatology, for example, antibody-based therapeutics have transformed disease. Anti-TNF [tumor necrosis factor] treatments can really lead to sustained remission, and if you had asked me if that was going to work well, I think I would have said “No,” but it’s actually life changing. I will say I sit in your skeptical camp, but I’m also happy to be taught otherwise by the real world.

Chris:
It’s what makes medicine and research so exciting and interesting: no end to having our paradigms overturned and new knowledge and new opportunities for prevention and treatment in HIV.

Eileen:
Chris, do you feel like you have a good handle on bNAbs now for when they emerge onto our therapeutic landscape?

Chris:
Yes, so both when and if they become available in the HIV treatment or prevention space, as well as guiding my patients who are interested in clinical trials that may involve bNAbs in terms of some of the risks and other considerations they should have. So, thanks so much for educating me. I hope listeners have also learned from this.

Eileen:
Chris, thanks for this really great discussion. To summarize, broadly neutralizing antibodies are antibodies that can stop new rounds of infection from a broad range of HIV strains. They’ve been derived from studies of people living with HIV who develop them naturally. So far, we can’t induce them with vaccines, but we’re working on it. They’ve been tried in prevention, in cure, and most recently in a therapeutic trial for every-six-month administration, and we expect that providers will see this as a possibility at some point in the next few years, although with a really unclear population for whom it will be most useful. To our listeners, thank you for joining in on another episode of Viremic. Please send any comments or questions you have to viremicpodcast@jh.edu, and we’ll be back in two weeks to talk about low-level viremia with our guest, Dr. Francesco Simonetti.

Announcer:
Viremic is sponsored by the Clinical Guidelines Program, a collaborative effort of the New York State Department of Health AIDS Institute and the Johns Hopkins University Division of Infectious Diseases.

Visit the program’s website at: HIVguidelines.org.

Viremic’s case discussions are for informational purposes only and not offered as medical or clinical practice advice for patients or clinicians. Any mention of specific medications or commercially available products is a description of use only, not an endorsement

The podcast is produced and edited by Jen Ham and Brian Hatcher with assistance from Jesse Ciekot and Laura LeBrun Hatcher.