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. Christopher Hoffmann:
Welcome to Viremic. I’m Chris Hoffmann and I’m joined today by my friend and colleague, Eileen Scully. Both of us are based in Baltimore at Johns Hopkins. Before we start, if you like this podcast, please share with a colleague and follow us wherever you access podcasts. In addition, we love hearing from listeners. Please send questions or future topic suggestions to us at viremicpodcast@jh.edu.

Eileen, it’s great to be recording today with you after a number of guest recordings. I really appreciate hearing your perspective and learning from you, and I’m looking forward to today’s discussion.

Dr. Eileen Scully:
Chris, it’s great to be back together and also to return to our patient-centered discussions about just what happens when you’re caring for patients in the clinic.

Chris:
I wanted to discuss a switch for a patient with an undetectable viral load. This is a very common situation for me. The patient that I’m going to describe is an amalgam of a number of patients, but also just a very common scenario of a patient who has been on multiple complex regimens and now I want to consider something simpler for reasons that we’ll get into. I’ve become more comfortable with these sorts of switches from complex multi-agent regimens to fixed dose combination regimens despite previous drug history and patterns of resistance.

Are most of the switches you make also among people with an undetectable viral load?

Eileen:
It’s a good question, Chris. I would say in my practice, it’s probably about 75% of the time that I change a regimen for a stably suppressed person. I do still have a good 25%, maybe 30%, for whom we’re changing for other reasons, either emergent resistance or intolerance. But I agree with you that the vast majority, thank goodness, are people who are suppressed and we’re just looking to further optimize.

Chris:
It’s great hearing your perspective because I know that our patient populations are somewhat different. So, getting onto this case, I have a 62-year-old man who was diagnosed with HIV in the early 1990s with a nadir CD4 count at that time of 135 and a diagnosis shortly thereafter of pneumocystis pneumonia. He’s been on and off of multiple regimens. His first regimen was dual NRTIs with lamivudine and zidovudine, followed by DDI and D4T or stavudine and hydroxyurea. He actually achieved transient viral suppression on the regimen of DDI/D4T/hydroxyurea, but eventually had viral load rebound and also struggled with the tolerability of that regimen due to fatigue and anemia.

This led to a gap in his antiretroviral therapy until about the late 1990s when he was started on boosted saquinavir, stavudine, and lamivudine. About a year later, this was switched to boosted saquinavir and efavirenz with no NRTIs at that time because of identified NRTI resistance on HIV resistance testing.

He did achieve viral suppression to some degree but never achieved a viral load below 500. The therapy was eventually stopped to try to prevent the emergence of additional HIV drug resistance.

I’m going to pause for a moment and see if you have any reflections at this point, Eileen.

Eileen:
Thanks, Chris, for that history. This takes us back to a time where, at times, the therapies were almost as toxic as the disease itself. When we think about how difficult it was to tolerate things like DDI and D4T and the toxicities of medications like hydroxyurea, I think it points out that, around that time, one of the things that we often had to do was to decide whether maintaining a regimen where you weren’t achieving suppression was really beneficial for the patient or was exposing them to more risk.

Fortunately, this isn’t something that we have to deal with very frequently in the modern era, but it is interesting to think about how far we’ve come in just the last 20 years, where now our medications are so much better tolerated and it would be extremely rare to take a position of not treating anyone, because even if you felt like they were unable to fully take their regimen and you were worried about resistance, we have so many things to choose from that usually you can find something that you feel comfortable giving. So, what one might say is a bit of a blast from the past, but it does also lead us to any treatment decision we make now will be in the context of someone who’s had a lot of toxic drug exposures and likely a lot of accumulated resistance.

Chris:
Thanks for that reflection, Eileen. I think it’s so helpful to ground ourselves in the journey of the patient and then also in making recommendations for a future regimen.

Moving on with his clinical history. In 2005, he was restarted on antiretroviral therapy with boosted lopinavir, efavirenz, fosamprenavir (back in the day that dual PIs were in vogue), and tenofovir/FTC. On that regimen, his viral load finally suppressed to less than 50, and his CD4 count was generally over 450. After quite a few years on that regimen, he was switched to TDF/FTC/boosted darunavir/raltegravir due to concerns for possible efavirenz- related fatigue.

He was switched again to boosted darunavir plus lamivudine plus dolutegravir due to kidney concerns with the TDF. Unfortunately, he didn’t tolerate the dolutegravir due to headaches and was switched within a week or two to boosted darunavir plus etravirine on which he achieved and maintained an undetectable viral load.

How do you synthesize the history up to this time?

Eileen:
Well, it sounds like someone who really engaged in care. When I say that, I mean, he took very difficult-to-take regimens and achieved viral suppression or near suppression, implying that he really is an active participant in his health care.

With the advent of the newest agents, it does seem like we were able to get him to a more tolerable regimen, although still with a boosted protease inhibitor included currently, and that he had some intolerance of dolutegravir, when dolutegravir and raltegravir were first emerging. There were some reports of CNS side effects; headaches and occasional mood changes are among those that people have reported. So not shocking, but now it seems like he’s probably been in kind of cruise control on this well-suppressive regimen, which is atypical, and not one that’s been really specifically studied, but has worked for many patients.

Chris:
Yeah, certainly not a regimen that I would go to these days. It was partly selected based on some of his HIV drug resistance mutations. In terms of reverse transcriptase resistance mutations that were identified over time, he has the M184V, 41L, 67N, 70R, 215F, 219Q, and the 103N. That includes both some TAM1, TAM2 pathways, and obviously the 184V. There were also some PI mutations that I don’t think we need to discuss given the path this case will take. But can you reflect on what these reverse transcriptase mutations mean to you?

Eileen:
The TAM pathways that you mentioned are thymidine analog mutation pathways, and those were selected by earlier generation NRTIs. There are two pathways that generally the virus went down, and it was felt that one was more favorable in terms of its cross-resistance profile, specifically to tenofovir, and the other conferring higher-level resistance to tenofovir, so we’re a little bit more concerned or watchful for it. That one is the 41/210/215 combination.

Classically, we’re taught that you either choose one or the other. In many cases, the patients “don’t read the books.” This patient has mutations from both of the pathways, so both the higher cross resistance and the lower cross resistance, but regardless, has some cross resistance to tenofovir. And then the M184V is the signature mutation to 3TC or emtricitabine and that emerges rapidly after the onset of non-suppressive therapy in the presence of either of those drugs.

It has 2 effects, one of which is to confer resistance to the medication, but the other is to reduce the replicative fitness of the virus. So, it’s a little bit less efficient at replication. So overall, definitely someone who’s had a lot of exposure to NRTIs and they are compromised. He also has within the reverse transcriptase the 103N, which is the signature mutation for efavirenz and confers high level resistance to efavirenz, but fortunately not too many of our more modern generation of non-nucleoside reverse transcriptase inhibitors.

Chris:
One of the reasons that this patient and many of my patients who are on somewhat atypical and perhaps more cumbersome regimens remain on them is because they are a little concerned about a change given a long history of difficult-to-tolerate regimens that were not completely effective.

So, for that reason, he hasn’t wanted to switch, but things recently changed when he was diagnosed with a pulmonary embolism (PE) and needed to be started on anticoagulation. In the hospital, he was started on apixaban with a dose reduction of 2.5 milligrams twice daily instead of the standard PE dose of five milligrams BID due to the drug-drug interaction with boosted darunavir.

I’ll pause for a moment and get your reflections on managing anticoagulation in patients on antiretroviral therapy and especially those on boosted protease inhibitors.

Eileen:
Great question and one that comes up all too frequently, especially as our patients here in the United States get a little bit older.

There are 2 concerns here. One is certainly the boosted PI, but the other one is etravirine or “etravirine,“ which has a brand name of Intelence. This is a medication that came out as an alternative to our first generation NRTIs and retained activity against some of those early mutations that commonly emerge to efavirenz or nevirapine, so it was very useful as we built salvage regimens in that time period. It has some advantages, one of which is that it can be dissolved and drank as a slurry. So, for people who have a very strong aversion to taking pills, it has that advantage. The disadvantage is that it has multiple drug-drug interactions. This is because it is both an inducer and an inhibitor of the cytochrome system, such that it can have difficult-to-predict drug-drug interactions, including with a variety of different anticoagulants. In general, this is a medication that I more actively try to get people off of because of the challenges of making sure that nobody adds on something that would have a drug-drug interaction with it.

Moving on from that, there’s the boosted protease inhibitor, darunavir/ritonavir, and this is in part because you cannot co-administer cobicistat with etravirine because of the interaction between the 2 drugs. Ritonavir classically has always been our most common drug-drug interaction, and comes up in a variety of cases, including with things like corticosteroids, which [you] can get topical administration and [have] systemic exposure.

But with the anticoagulants, it has become an increasing problem. As you mentioned, there is guidance for dose reducing apixaban to 2.5 milligrams BID, and that being considered acceptable. Now, apixaban and rivaroxaban are our [Factor] Xa (pronounced 10A) inhibitors, and dabigatran is a direct thrombin inhibitor, all of which are in the direct oral anticoagulant category and are used as essentially replacements for coumadin or warfarin.

One of the challenges around this is that while there is some therapeutic drug monitoring that can be done for Xa inhibitors, it’s not standardized. There aren’t good reference ranges and there aren’t necessarily targets. So, when we know there is a drug-drug interaction and we’re not able to accurately predict exactly what it is, it can leave us feeling a little bit uncomfortable with what level of anticoagulation we’re actually achieving. With warfarin or coumadin, we directly measure this with INRs. With the DOACs, you don’t have to, but it does leave me feeling a bit uncomfortable with the long-term combination of these direct-acting anticoagulants and with boosted protease inhibitors. How do you feel about it, Chris?

Chris:
I share your same feelings. In the European [guidelines] and some other regulators recommend against co-administration of ritonavir with apixaban.

Thanks for raising the issue of etravirine. For my patients who are discharged from the hospital or with a medication added by a subspecialist, the most common drug-drug interaction that is overlooked is between the etravirine and whatever new drug was added. And I think with the apixaban, as you highlighted, this is another example of that.

I prefer to use warfarin if I cannot switch off of a boosted protease inhibitor or a more complicated regimen that may have additional drug-drug interactions, like one with etravirine. Obviously there are challenges with patient satisfaction with that, and warfarin is a drug with considerable risk of either over- or anti-coagulation depending on changes in diet and other factors. So, when I can, this is where I look for a switch in the antiretroviral regimen to one that is compatible or more compatible with apixaban or whatever other anticoagulation is being used.

Eileen:
Chris, I think that’s a great approach. We’re used to as physicians managing the fact that when you need anticoagulation, you get a risk of bleeding, and also the fact that Coumadin or Warfarin values are challenging to manage sometimes, especially in people who don’t have a totally stereotyped diet. The difference here is that with Coumadin, we have to accept that that’s part of the process. Whereas with DOACs, we can reliably achieve a certain level as long as we don’t have a drug-drug interaction. I think [that] puts the ball back in our court to try to find the safest possible combination.

Chris:
Let’s move on to figuring out what the right combination could be for this individual or some options for combinations that get away from those drug-drug interactions.

Maybe it’s useful to mention his HIV drug resistance mutations again: There’s the M184V, which confers high-level resistance to lamivudine, but also has a viral fitness cost to the virus, so reduces the replicative activity. Then there are the TAM1 and TAM2 pathway mix of mutations that lead to resistance to a number of NRTIs, classically zidovudine and stavudine, but also with cross-resistance to tenofovir and other NRTIs. Those include the 41L, 67N, 70R, 215F, and 219Q. There’s also the 103N with high level resistance to efavirenz and nevirapine.

After reviewing these mutations and his treatment history, what approach would you take to his ART options?

Eileen:
Chris, just one more clarifying question. You mentioned in the original history that at some point it looks like he was put on a tenofovir-sparing regimen, but in part, I think it said something about kidney concerns.

In the past, we sometimes viewed tenofovir disoproxil fumarate as something that needed to be removed in people with evolving renal function or at risk of kidney disease, and in particular, when that medication was going to be combined with a boosted protease inhibitor. I’ll put a little footnote here that as we consider the new regimen for this individual, they do have some cross resistance to tenofovir, although we’ll still likely have some activity. With the tenofovir-alafenamide formulation, a lot of us are much more comfortable with using it in people who are either at risk of kidney disease or have some degree of kidney disease. That’s one thing that I would put back into the mix as we’re thinking about changing this patient.

As you’ve already introduced, when is there a reason to change a therapy? Often the reason is that the patient requests some easier to take, less frequent, smaller pill size, some side effect. That’s one of the primary reasons. But also, if the regimen is complex, I’m sure we’ve all had the experience of where only one of the medications is refilled and then the patient is at risk because they didn’t get them all at one time. So, these simplification steps that can eliminate some inherent risks of treatment being complex.

And then also the drug-drug interaction, which here, clearly, while we’ve talked about how this is possible, and if you only can tolerate a PI, there is a pathway that is FDA-approved to use DOACs together with that. If we have other options, it’s a very reasonable time to explore them. So that’s where I would be starting as I think about this. What about you, Chris?

Chris:
So helpful to go through a checklist of “Is there a reason to change?”:
• Certainly, there’s not treatment failure. He is on a non-standard regimen but has been doing well and has been tolerating the need to take multiple tablets.

• He has not experienced any notable side effects recently. This regimen is not known for any specific long-term toxicity.

• But as you raised the issue, there are certainly important drug-drug interactions here that could be reduced potentially with a different regimen.

• There are additional comorbidities that come with aging, but none that really affect regimen selection. For example, his EGFR is >60. He does not have known cardiovascular disease or diabetes or other risk factors for kidney disease or liver disease.

• Since we’re talking about drug-drug interactions, I think it’s useful to consider what other drugs he’s on. Besides the apixaban, none of the other drugs that he’s on are cleared through any of the cytochrome P450 pathways or have any other significant drug-drug interactions with antiretroviral therapy.

Eileen:
Well, that’s a great point, Chris. We’ll highlight here that when you’re taking people off of something, you should also consider that you’re impacting potential drug exposures to other components in their existing regimen.

I think about this frequently for opiate use disorder therapy, where when you discontinue a protease inhibitor or something like etravirine, you may change the effective exposure to other medications. So be mindful of that. If people start to report early withdrawal symptoms or something similar to have some sort of anticipatory management that that may actually happen. We often think about the interactions when we add a medication, but they also can be relevant when you take one away.

Chris:
If we move on to a potential switch, I consider which medications I want to avoid, which medications may still be effective given the pattern of resistance, and which medications there may be already a side effect history for, which is a reason to avoid, such as the dolutegravir, to which he had developed headaches at one time.

One of the things I do is I put in the resistance pattern, current regimen, comorbidities into HIVassist.com, which is a really helpful tool to show which regimens have the best evidence base, usually from clinical trials for effectiveness in that scenario. Sometimes I note something that I wasn’t thinking about then that may actually be the optimal regimen for my patient.

The other thing beyond that is to remember that although we have a lot of great agents, it’s good to think about where the data are also. In the past, there have been some good thoughts that clinical trials have shown were probably not the right way to go, including combinations of boosted darunavir and raltegravir. Some of the trials with boosted darunavir monotherapy or lopinavir monotherapy are reasons to pause before jumping into something in a data-free way.

Fortunately, we do have data on regimens that could work for my patient and studies since those that I mentioned on simplification have pointed away. I thank the investigators who have led those studies in providing the data that we have now.

So, I’ll pose a question for you, Eileen. Can we get him on a single pill regimen?

Eileen:
Great question. To summarize, we have a fully suppressed individual currently on darunavir, boosted with ritonavir, plus etravirine, history of nuc [NRTI] resistance, and we’re looking to make a switch to have a good tolerability profile with a direct acting oral anticoagulant. So, it’s going to push us away from protease inhibitors, as you’ve already mentioned, towards non-protease inhibitor-based regimens, which include our integrase inhibitors and NNRTIs. That’s where we come to a split in the road. We know that there’s background nuc resistance, and that an integrase inhibitor combined with nucs, even in the setting of resistance, has efficacy. We’ll go through some of the studies that show that.

We have much less data to support that approach using nucs with an NNRTI when the NNRTI you believe to be fully active, but the nucs have compromised. That has not been overall a strategy that’s been well tested. In this case, our non-nuc options would be rilpivirine or doravirine, outside of etravirine, which we’ve already mentioned has some of its own drug-drug interaction complications. But those 2 as the backbone of the regimen would not be ones I would feel comfortable with (from a data perspective) using in combination with nucs when we know that there’s background nuc resistance.

In contrast, I feel pretty good about using an integrase inhibitor with this level of nuc resistance. Where do I get this good feeling from? There’s a couple of places; one is that we know that strategy actually works in people who failed treatment. In the NADIA trial, which was published in 2022 in the New England Journal, they looked at individuals who had failed their first-line therapy—an NNRTI plus 2 nucs strategy for first-line therapy and then randomized to either receive dolutegravir plus 2 nucs or darunavir boosted plus 2 nucs, and look to see whether or not they were able to achieve viral suppression. In this population, they saw very high levels of resistance to the background nucs with upwards of 90% with an M184V or I mutation and a very substantial proportion of them also with a K65R mutation, which is a signature tenofovir resistance mutation. Despite this high level of nuc resistance, they saw very high levels of viral suppression with either dolutegravir or darunavir.

Now I should note that this is a bit different. This is a re-initiation scenario where the individuals were viremic. But to me, that’s just even stronger evidence because when you’re making a switch in an already suppressed person, the barrier to overcome the drugs is even higher. Would you agree with my interpretation of that study?

Chris:
We learned so much from NADIA and the subgroup analysis comparing viral load suppression among individuals who had essentially zero predicted active NRTIs versus those who had one or two predicted active NRTIs showing similar rates of suppression, to 90% in both the dolutegravir and boosted darunavir arms. [It] really shows that compromised nucs do not necessarily compromise the regimen when used in combination with an agent like dolutegravir or boosted darunavir.

Eileen:
You make a really important point there, Chris, in that you’ve already mentioned that monotherapy studies have in general not done well. One important point here is that while we are saying that there is resistance to nucs, we’re making a very clear distinction that we don’t think this is the same as only having a single drug on board. That despite the presence of some resistance, there is still some residual activity of those drugs. That makes the overall strategy much more successful than monotherapy.

Chris:
Definitely, and that gets back to basing our decisions on data and not making extrapolations that may seem reasonable but may lead us down the wrong path.

Another study worth mentioning is one looking at bictegravir. We’ve had several studies on dolutegravir in patients who have prior treatment and substantial NRTI resistance, but there was a study completed in Haiti looking at bictegravir/TAF/FTC switch for people with an undetectable viral load who were on second-line therapy. This is a little closer to my patient in that he has an undetectable viral load.

In that study, there were about 300 participants assigned to either the bictegravir/TAF/FTC, or a boosted protease inhibitor. Both arms performed very well. In this study, rather than standard genotyping, they had baseline proviral HIV drug resistance testing, and in the bictegravir group, about half of the participants had proviral demonstration of 184V or I mutation, and about 16% [had] 65R, the tenofovir mutation. Essentially, 90 some percent of individuals suppressed and [that] was not different by the presence of those mutations. So, this was additional data that helped reassure me that not just in dolutegravir, but also in bictegravir and in two different settings, one in Sub-Saharan Africa and one in Haiti, with somewhat different prior treatment management, a similar success despite the presence of background NRTI resistance.

Eileen:
I totally agree, that study is very reassuring and speaks to the fact that for a long time we only considered boosted protease inhibitors to be strong enough to handle the second-line patients, but we now know that our current generation of integrase inhibitors, dolutegravir and bictegravir, which are considered to be very equivalent in many ways (so we do a little extension of the data from one to the other) are really strong partners for situations where you have some background resistance and you need a very strong anchor drug in your regimen.

Chris:
I wanted to mention that there certainly are other studies that further help support the use of one of our second generation INSTIs, dolutegravir or bictegravir, in the setting of background NRTI resistance, especially the 184V. There are a number of cohort studies in which individuals either on dolutegravir plus lamivudine or dolutegravir plus two NRTIs have had resistance and many of the individuals have done well. Cohort studies do have limitations. One is that people who don’t do well are often switched off, perhaps before they’re included in the cohort, and the other is that without randomization, you’re looking at people who have had a prior challenge with adherence and developed the resistance and may have future challenges with adherence that have nothing to do with the effectiveness of the drug.

I did want to have you comment on the potential role of lamivudine even in the setting of high-level resistance and the possible impact of maintaining a 184V mutation.

Eileen:
This is one of those questions that never really goes away. There is data to show that the M184V makes the virus less fit. Back before we had fully suppressive therapy, in situations where we had nothing else to offer, if you gave someone who had a documented M184V 3TC as a therapeutic, you would get a slight decline, about a half log in the viral load decline, even without achieving full viral suppression. That did have some benefit of slowing the rate of decline of CD4 cells. So, we know that something happens when you’re exposed to it, either because you’ve just forced the virus to be a little bit less efficient or because the drug is having some effect. This has led many people to consider keeping 3TC in regimens, even in the context of an M184V, either for enhancing the regimen or, as we used to say, push the virus towards this less fit phenotype.

Now, in the setting of full suppression, it’s not clear what a less fit phenotype really means. You’re not replicating, so it should not matter. So, it is still an open question as to whether or not 3TC is of benefit in this setting. The studies we’ve already discussed, which have shown that therapy, including a 3TC component, is efficacious and is substantially more efficacious than monotherapy, but we don’t know exactly which components are driving that. In almost all cases, it’s paired with tenofovir. So, it’s hard to say whether or not we think that the 3TC or the tenofovir or the combination of the 2 is what’s having the effect.

So, what I’ll say is 3TC has a very favorable toxicity profile, meaning it’s pretty hard to show true harm from it as a medication, and there is enough evidence to suggest that it does still do something, even when resistance may be present, that I’m relatively hard pressed to drop it from regimens unless it is a matter of convenience, that it’s simply too hard to continue to take it. I’m not sure that the data totally supports my opinion on that. There’s been a couple of trials that have looked at keeping it or dropping it, and I don’t think many of them have shown definitively that it’s helpful, but in my practice in general, it’s also not been harmful. What’s your approach on that one, Chris?

Chris:
I think 3TC or lamivudine is the favorite HIV medication of HIV providers—may not be as potent as an INSTI or boosted darunavir, but has minimal toxicity and always seems to help things get a little bit better in terms of viral suppression. As you did highlight, there are a few studies that do suggest that dropping lamivudine, even in the setting of the M184V, may lead to worse outcomes.

[There are] a couple of studies looking at either monotherapy or maintaining NRTIs. One that I will mention is the MOBIDIP, looking at boosted protease inhibitors, either darunavir or lopinavir, about half and half, plus or minus 3TC. There was considerable failure with the monotherapy—about 20% compared to about 2% with the boosted protease inhibitor that included 3TC. It was a fairly small study, but since I already have a bias towards liking lamivudine it helps to reinforce that bias.

I don’t know if you have any other comments on M184V and maintaining lamivudine or not.

Eileen:
That pretty much encapsulates it for me as well.

Well Chris, we don’t know what you did for this patient. So here you’ve got an M184V. You want to switch away from your boosted protease inhibitor regimen. One of the tantalizing options would be bictegravir plus FTC plus TAF. So, what did you do?

Chris:
I did exactly that: BIC/TAF/FTC. I avoided dolutegravir because he had the headache with that. So that was not an option. And based on the studies that we talked about, especially the NADIA and the Haiti study, despite the fact that he has fairly high level NRTI resistance mutations, I was comfortable switching him to a single tablet regimen of BIC/TAF/FTC.

Eileen:
I would imagine that this was pretty exciting for this patient.

Chris:
Yes, this has been somewhat of a recurring theme with a number of my patients who have a long history of living with HIV and an attachment to some regimen that is often not so convenient. When they finally are ready to switch or push to switch for medical reasons, they’re often very thankful that they’re on a new, simpler, and easier to take regimen.

Eileen:
That’s great.

Chris:
Eileen, this has been a fun discussion. I always gain new insights when talking with you about ART regimens and care of people living with HIV, and I’m sure our listeners have also learned from you. Thanks so much.

Eileen:
Well, thanks, Chris, and thanks for surfacing this really important question. Maybe in some future case, we’ll also talk about whether or not we should be waiting for the pulmonary embolism to push us to do this and the barriers on the provider side for us to think about doing this even earlier for our patients.

Chris:
I love that point.

To our listeners, thanks for joining another episode of Viremic. Please send any comments or questions to viremicpodcast@jh.edu. We’ll be back in two weeks with a case involving HIV management considerations for a patient with Kaposi’s sarcoma.

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