• Host Factors in the Pathogenesis of HIV Disease: Implications for Therapeutic Strategies (S16)
  Authored by Anthony S. Fauci
  View the original abstract

• Latent Reservoir and Residual HIV-1 Replication on Antiretroviral Therapy (S17)
  Authored by D. D. Ho, B. Ramratnam, M. Louiie and M. Markowitz
  View the original abstract

Some further insights into treatment interruptions and philosophies of treatment. Dr. Anthony Fauci in his talk on viral reservoirs focused on issues surrounding treatment interruptions. He highlighted three reasons why treatments interruptions are of interest:

1. to attempt to auto-vaccinate patients to stimulate anti-HIV immunity;

2. in an effort to shift to wild type drug sensitive virus in the setting of salvage therapy; and

3. to decrease drug exposure.

He expressed skepticism about the merit of the auto-vaccination concept and supported more work in the setting of salvage therapy. He was more positive about efforts to creatively utilize treatment interruptions as a mean to minimize exposure to drugs and presented preliminary data on two studies where HAART was being cycled either two months on and one month off or one week on and one week off. In the next talk, David Ho (abstract S17) presented data suggesting that current HAART regimens are not maximally suppressive (he estimated perhaps 20% less than 100% suppressive) and expressed optimism that more potent regimens might speed up the decay rate of virus in reservoirs.

For me, that talk underscored the need to creatively improve both the potency of our therapies and our approach to most effectively utilizing the drugs to provide clinical benefit over the longest time period possible. With all of the interest in treatment interruptions, it would be useful to have a better understanding of what happens when effective treatment is stopped for a prolonged period of time. Pablo Tebas and colleagues summarized their experience with 31 patients who stopped HAART after durable full expression had been achieved. The patients had a low nadir CD4 count prior to HAART of 383 cells/mm³ and a baseline viral load= 30,000 copies/ml/. With an average follow-up period of 50 weeks, the CD4 cells declined at an average rate of 16 cells/mm³ and the viral load rebounded to within 0.5 log of their baseline in all cases. The rate of decline of CD4 count was related to the increase in CD4 cells experienced with HAART. Those data provide a framework to start better understanding the dynamics of novel approaches to treatment whereby the CD4 count might be used to determine when to start and stop potent antiretroviral therapy.