Careers  |   Log In  |   Register  |   Welcome Center  |   Follow Us  Facebook  Twitter Google Plus

Second-line anti-retrovirals suppress resistant HIV

NEW YORK (Reuters Health) – African patients with resistant strains of HIV had favorable results from second line protease-inhibitor-based anti-retroviral therapy (ART), with no increase in drug-resistant HIV mutants.

The findings “are clinically significant because they indicate expected treatment response in patient switched to second-line HIV treatment without genotypic resistance testing, as is the reality in resource-limited settings,” lead researcher Dr. Kim Sigaloff from the University of Amsterdam told Reuters Health.

Conducted at 13 sites in Kenya, Nigeria, South Africa, Uganda, Zambia and Zimbabwe, the prospective study involved 243 adults who were switched to a second-line protease-inhibitor (PI)-based regimens following first-line treatment failure.

Among the 208 patients who continued second-line ART for at least a year, 28 (13.9%) had virological failure, defined as HIV RNA counts of 400 copies/ml or more.

Twenty-one patients (12.1%) had immunological failure, defined as CD4 cell counts persistently <100 cells/cu mm or a decline of more than 50% from peak levels during treatment.

Before patients were switched to the second-line drugs, the researchers had looked for drug resistance mutations; they found that in 55.2% of patients, the second-line drugs were likely to be only partially active. Resistance to nucleoside analog reverse transcriptase inhibitors (NRTIs) and non-NRTIs was predominant.

“Our study demonstrates that empirically prescribed PI-based regimens can successfully re-suppress HIV, even in the absence of a fully-active NRTI backbone,” the researchers said in a March 23 online report in the Journal of Infectious Diseases.

On multivariate analysis, virological failures were significantly linked to treatment compliance but not to the predicted activity of second-line regimens.

“The good immunological and virological response to partially-active second-line regimens, i.e. in participants who harbored NRTI resistance, is likely explained by the high potency and genetic barrier to resistance of ritonavir-boosted protease inhibitors,” the researchers suggest.

They conclude, “Our data suggest potential for the use of simplified PI-based regimens after failure of an (non-NRTI)-based regimen.”


J Infect Dis 2012.