A common mechanism of clinical HIV-1 resistance to the CCR5 antagonist maraviroc despite divergent resistance levels and lack of common gp120 resistance mutations

Michael John Roche, Hamid Salimi, Renee Charlene Duncan, Brendan Wilkinson, Kelechi Chikere, Miranda S Moore, Nicholas Webb, Helena Zappi, Jasminka Sterjovski, Jacqueline Kaye Flynn, Anne Ellett, Lachlan Robert Gray, Benhur Lee, Becky Jubb, Mike Westby, Paul Allen Ramsland, Sharon Ruth Lewin, Richard J Payne, Melissa Churchill, Paul R Gorry

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The CCR5 antagonist maraviroc (MVC) inhibits human immunodeficiency virus type 1 (HIV-1) entry by altering the CCR5 extracellular loops (ECL), such that the gp120 envelope glycoproteins (Env) no longer recognize CCR5. The mechanisms of HIV-1 resistance to MVC, the only CCR5 antagonist licensed for clinical use are poorly understood, with insights into MVC resistance almost exclusively limited to knowledge obtained from in vitro studies or from studies of resistance to other CCR5 antagonists. To more precisely understand mechanisms of resistance to MVC in vivo, we characterized Envs isolated from 2 subjects who experienced virologic failure on MVC.
Original languageEnglish
Pages (from-to)1 - 20
Number of pages20
Issue number1 (Art. No.: 43)
Publication statusPublished - 2013

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