TY - JOUR
T1 - Mutations selected in HIV-2-infected patients failing a regimen including atazanavir
AU - Cavaco-Silva, Joana
AU - Aleixo, Maria João
AU - Van Laethem, Kristel
AU - Faria, Domitília
AU - Valadas, Emília
AU - Goncalves, Maria de Fátima
AU - Gomes, Perpétua
AU - Vandamme, Anne Mieke
AU - Cunha, Celso
AU - Camacho, Ricardo Jorge
N1 - Funding Information:
This work was supported by Fundac¸ão para a Ciência e Tecnologia (FCT) (PhD grant no. SFRH/BD/61141/2009 to J. C.-S.) and by the European Commission’s Seventh Framework Programme (FP7/2007-2013) under the project ‘Collaborative HIV and Anti-HIV Drug Resistance Network’ (CHAIN, grant 223131).
PY - 2013/1
Y1 - 2013/1
N2 - Objectives: To investigate mutations selected in viruses from HIV-2-infected patients failing a highly active antiretroviral treatment (HAART) regimen including atazanavir/ritonavir. Methods: Twenty-eight HIV-2-infected patients previously exposed to atazanavir/ritonavir and failing therapy were studied. The protease (PR) gene was amplified and sequenced, and mutations emerging under atazanavir/ritonavir selective pressure were reported. Results: The I50L mutation emerged in 4 out of 28 HIV-2-infected patients failing a HAART regimen including atazanavir/ritonavir. Besides I50L, four PR mutations previously associated with protease inhibitor resistance (I54L, I64V, V71I and I82F) and six PR mutations of unknown impact (V10I, E37D, S43T, K45R, I75V and F85L) in HIV-2 were also identified in this small group of patients. Conclusions: Several mutations were associated with virological failure of a regimen including atazanavir/ritonavir in HIV-2-infected patients, including I50L for the first time. It should be included in HIV-2 algorithms for interpretation of genotypic resistance data, and taken into account when making therapeutic decisions for HIV-2-infected patients.
AB - Objectives: To investigate mutations selected in viruses from HIV-2-infected patients failing a highly active antiretroviral treatment (HAART) regimen including atazanavir/ritonavir. Methods: Twenty-eight HIV-2-infected patients previously exposed to atazanavir/ritonavir and failing therapy were studied. The protease (PR) gene was amplified and sequenced, and mutations emerging under atazanavir/ritonavir selective pressure were reported. Results: The I50L mutation emerged in 4 out of 28 HIV-2-infected patients failing a HAART regimen including atazanavir/ritonavir. Besides I50L, four PR mutations previously associated with protease inhibitor resistance (I54L, I64V, V71I and I82F) and six PR mutations of unknown impact (V10I, E37D, S43T, K45R, I75V and F85L) in HIV-2 were also identified in this small group of patients. Conclusions: Several mutations were associated with virological failure of a regimen including atazanavir/ritonavir in HIV-2-infected patients, including I50L for the first time. It should be included in HIV-2 algorithms for interpretation of genotypic resistance data, and taken into account when making therapeutic decisions for HIV-2-infected patients.
KW - HIV-2
KW - Protease
KW - Resistance
UR - http://www.scopus.com/inward/record.url?scp=84871227694&partnerID=8YFLogxK
U2 - 10.1093/jac/dks363
DO - 10.1093/jac/dks363
M3 - Article
C2 - 22977160
AN - SCOPUS:84871227694
SN - 0305-7453
VL - 68
SP - 190
EP - 192
JO - Journal of Antimicrobial Chemotherapy
JF - Journal of Antimicrobial Chemotherapy
IS - 1
ER -
