On Thursday afternoon, under Theme B: Antiretroviral Therapy, things moved up a gear, with back to back presentations touching almost every aspect of the ART and the long term complications. Dr David Nolan from Royal Perth Hospital gave a thoroughly captivating revision around HIV treatment. He gave a brief account of the pre, early and late HAART treatment options, how things have evolved in terms of the choices, co morbidities, tolerability and toxicity.
He reflected on the contemporary challenges around decision making in clinical practice, how we can factor in the newer therapies and novel diagnostic approaches in our existing treatment and screening paradigms.
What do we know that we do not know?
David argued that despite of having potent ARTs with superior virological efficacy, we don’t have enough evidence to guide us on how to screen, monitor, and subsequently manage the emerging associated co morbidities including HIV neurocognitive impairment, chronic immune activation, and increased risk of malignancies.
What don’t we know that we do not know?
David threw up some very topical questions with both ethical and public health implications. Does it matter that there are things we don’t know? Should we change ART regimen just because we have newer drugs? What if HIV patients with sustained viral suppression do not want to change their old medications?
These are very complicated and yet practical questions, and we still do not seem to have a simple answer. With discovery of newer, safer and simpler ART regimen, we are likely to find ourselves in a situation where we might simply not have enough evidence to guide clinical choices when it comes to changing or switching regimen. In that case he concluded that we might simply accept the fact that there will always be unknown unknowns.
He also discussed the rationale of ART treatment intensification (using Maraviroc for example) and what should be realistically expected. He pointed out that current evidence indicate that treatment intensification makes little difference in some of the important prognostic clinical parameters like viral load and immune activation markers. It does not appear to impact on viral reservoirs and residual viremia which tend to be established early following primary HIV infection. He posited that, in absence of robust evidence for treatment intensification, the seemingly logical approach will be to start treatment early following seroconversion.
This was arguably one the most thought provoking presentation I have attended in this conference. It raises some of the difficult issues clouding the field of HIV and ART treatment and long term treatment outcome. Obviously, there are things that we do know, and things we have been doing well in improving our knowledge and understanding of how ART works.
Perhaps, It is time to start thinking about how do we integrate the use of monocyte activations markers like sCD14, in the standard of care for our patients. For the next few years it will be pretty much about the known unknowns and the unknown unknowns that will really determine if we are going to win another important dimension of this epidemic when every HIV patient has undetectable viral load.