NEW YORK (Reuters Health) – An ultrasensitive assessment of HIV-RNA levels in HAART-treated patients with subclinical viral loads reveals that nevirapine-based regimens are more effective in this setting than those based on efavirenz or lopinavir/ritonavir.

The findings come from a study of 154 HIV-infected patients who were classified as full treatment responders as their HIV-RNA levels were below 50 copies/mL. While this has been the standard target for antiretroviral therapy, in the last few years, tests have become available that can detect HIV-RNA levels as low as 2 copies/mL.

As reported in the March issue of the Journal of Medical Virology, Dr. Stefano Bonora, from the University of Torino, Italy, and colleagues used an ultrasensitive assay (detection limit = 2.5 copies/mL) to assess HIV-RNA levels in the study group. The subjects included 48 treated with nevirapine, 57 with efavirenz, and 49 with lopinavir/ritonavir, in addition to two nucleoside/nucleotide reverse transcriptase inhibitors.

Overall, 60.4% of nevirapine-treated subjects, 42.1% of those given efavirenz, and 28.6% of those treated with lopinavir/ritonavir had undetectable HIV-RNA levels, i.e., below 2.5 copies/mL.

On average, the duration of virologic suppression (<50 copies/mL) was 28.6 months, the report indicates. In only the lopinavir/ritonavir group did the length of suppression correlate with a significantly lower viral load (p = 0.015). The average nadir CD4+ cell count was significantly lower with lopinavir/ritonavir than with the other agents. As virologic suppression increased, the CD4+ cell count rose in the nevirapine group, but fell in the lopinavir/ritonavir group. Regression analysis confirmed that nevirapine-based treatment was the only independent predictor of HIV suppression below the current threshold, the researchers note, “possibly due to its greater penetration in extra-vascular compartments. They conclude, “The clinical importance of this findings deserves further study in the context of persistent low-level viremia under long-term HAART and the impact of antiretroviral penetration into long-lived reservoirs of virus.” Reference:
J Med Virol 2009;81:400-405.