BACKGROUND: There are very few and contradictory data about the consequences of 'blips', transient rebounds of HIV viremia. We assessed the emergence of new drug resistance mutations during blips among HIV-infected patients on HAART from a cohort in which we found no association between blips and virological failure. METHODS: Seventeen patients with blips were selected from 330 patients under HAART for over 48 weeks according to these criteria: (1) presence of only one blip, viremia < or =1000copies/ml preceded by two consecutive visits and followed by one visit showing undetectable viremia; (2) therapy adherence > or =95%; (3) availability of frozen sera. RESULTS: HIV RNA could be extracted and amplified from five patients. In another two patients only the protease region could be amplified. Drug mutations in either the retrotranscriptase or protease genes, not detected at baseline, were observed in six patients at the blip. None of the patients showed detectable viremia during a median (range) follow-up after the blip of 120 (36-156) weeks. CONCLUSIONS: Transient rebounds of viremia in patients on HAART are associated with the emergence of new drug resistant HIV variants. In spite of it, virological failure is not observed after a median follow-up of over 2 years.
BACKGROUND: There are very few and contradictory data about the consequences of 'blips', transient rebounds of HIV viremia. We assessed the emergence of new drug resistance mutations during blips among HIV-infectedpatients on HAART from a cohort in which we found no association between blips and virological failure. METHODS: Seventeen patients with blips were selected from 330 patients under HAART for over 48 weeks according to these criteria: (1) presence of only one blip, viremia < or =1000copies/ml preceded by two consecutive visits and followed by one visit showing undetectable viremia; (2) therapy adherence > or =95%; (3) availability of frozen sera. RESULTS: HIV RNA could be extracted and amplified from five patients. In another two patients only the protease region could be amplified. Drug mutations in either the retrotranscriptase or protease genes, not detected at baseline, were observed in six patients at the blip. None of the patients showed detectable viremia during a median (range) follow-up after the blip of 120 (36-156) weeks. CONCLUSIONS: Transient rebounds of viremia in patients on HAART are associated with the emergence of new drug resistant HIV variants. In spite of it, virological failure is not observed after a median follow-up of over 2 years.
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