The Evolution of Antiretroviral Therapy for HIV - Episode 14
Peter L. Salgo, MD: Have you been using fostemsavir?
Paul E. Sax, MD: We have a patient congenitally infected. The individual is in his mid-20s, is resistant to all available drugs, is failing clinically, his CD4 is below 100, he has complications of AIDS, and he’s now on these drugs as part of clinical trials.
Joseph Eron, MD: We have a couple of people on the trial with fostemsavir. One is a woman who really had kind of crazy beliefs about how to take her medicine and also was stuck on zidovudine. And I think it was intolerable for her, but for whatever reason, she finally got referred to us. She’s on fostemsavir, she’s off zidovudine, and she’s suppressed. But one reason why she’s suppressed is she has a study coordinator that literally calls her every week and says, “Have you taken your pills this week?” And over the Christmas holiday, she came in early January with a detectable viral load because she didn’t get her phone call over the holiday. But it does work.
Peter L. Salgo, MD: Do you see these newer drugs as part of your armamentarium?
Joseph Eron, MD: I think so. And I think, again, we do. In clinic, we had, exactly, one of these young ladies that Paul was talking about—someone who’s been through so many regimens as a teenager. I mean, trying to get teenagers to do anything (eg, brush their teeth, dress appropriately) is difficult. Anyway, the point is, it’s tough to get adolescents to do anything, and then they’re HIV-infected. They have all that emotional and psychological baggage. They can have really resistant virus.
Peter L. Salgo, MD: Right. You were just pointing that out. These are the folks with resistant virus. And, in fact, as the population ages with the initial wave, you got control. Then, we’ve got the congenitally acquired folks who are resistant. But you’ve got that cohort.
Eric S. Daar, MD: That cohort will continue until they get suppressed and live forever or die.
Joseph Eron, MD: Right. And the other thing about it is, it’s not like if they go on the attachment inhibitor, fostemsavir, and it works, then they’ve got to stay on it. It’s not like there’s going to be a replacement any time soon.
Peter L. Salgo, MD: So what you’re saying is, if we control transmission at childbirth—we’ve got this cohort that has it, they’re resistant—they’re going to need something like fostemsavir or something like that?
Joseph Eron, MD: Right. I do have patients where I know that underneath the surface of the water, they have a lot of resistance. And when they come in and I get their viral load, I wait for that viral load. And I think, if their viral load is up, I don’t know exactly what I’m going to do.
Paul E. Sax, MD: Usually it’s because they had a hiatus in their therapy, fortunately. It’s very rare that they’ve now developed dolutegravir resistance. It can happen.
Joseph Eron, MD: But you can worry about that. Maybe I should stop worrying?
Eric S. Daar, MD: Keep worrying.
Paul E. Sax, MD: I do worry. We had someone who, inadvertently, didn’t have a prescription refilled properly. He was on twice-daily dolutegravir because he needed twice-daily dolutegravir. He had a lot of integrase resistance. With the wrong refill, he was given it once daily and he had virologic rebound. Fortunately, he did not have selection of new integrase resistance. Now he’s back on twice-daily dolutegravir and enfuvirtide, so he’s suppressed again.
Joseph Eron, MD: But, again, it’s one patient a month that one of us might worry about, not 3 patients a day. So, it is a small population.
Transcript edited for clarity.