Simon Collins, HIV i-Base

Vernazza and colleagues presented results looking at the compartmental effect of reducing treatment to ritonavir-boosted atazanavir monotherapy in 30 patients (28 male) suppressed to <50 copies/mL on triple therapy.

HIV viral load was measured every 4 weeks, and semen and cerebro-spinal fluid (CSF) samples were obtained from consenting patients at baseline (semen) and Wk24 (semen+CSF). The primary endpoint was defined as 2 consecutive viral load values >400 copies/mL.

One patient failed monotherapy at week 8 who was retrospectively shown to have previously failed a PI based HAART. One patient prematurely terminated treatment at week 20. All remaining 27 patients had suppressed viral load <100 copies/mL at week 24. 22 patients still remain on ATV/r with a median follow-up of 19 months (6 –29) and a mean CD4 increase of 78 cells/mL.

19 CSF samples were obtained at week 24, 3 patients had detectable HIV-RNA in CNS (2.2, 2.9, 3.8 log10 cp/ml) despite fully suppressed HIV-RNA in blood, although all three CSF samples were wild type. Viral load was undetectable in all semen samples (n=15).

The authors concluded “limited penetration of PI into CNS may result in replication of wild-type HIV in the CNS in a relevant subset of patients. As the consequence of low-level HIV replication in different compartments is not known, future monotherapy trials should include careful monitoring of compartments other than blood. Mono-maintenance, however, might be a valid option for future studies.”

Ref:

Vernazza P, Daneel S, Schiffer V et al. Risk of CNS-compartment failure on PI monotherapy (ATARITMO-study). Poster abstract WEPE0073.