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Journal of Clinical Microbiology, February 2004, p. 862-866, Vol. 42, No. 2
0095-1137/04/$08.00+0 DOI: 10.1128/JCM.42.2.862-866.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Service of Infectious Diseases, Hospital Carlos III, Madrid, Spain,1 ViroLogic, South San Francisco, California2
Received 29 April 2003/ Returned for modification 11 July 2003/ Accepted 29 October 2003
A total of 76 patients discontinued treatment with didanosine plus hydroxyurea after 1 year of maintenance therapy. The greatest human immunodeficiency virus (HIV)-RNA rebounds were seen in 10 patients harboring an L74V mutation, and the presence of viruses with this mutation rapidly waned. In contrast, viral rebounds were significantly less pronounced (P < 0.01) in 12 subjects harboring thymidine-associated mutations; these mutations persisted in all instances. Thus, selection of an L74V mutation during didanosine therapy may compromise HIV replication in vivo.
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