Journal article
Frequency and Env determinants of HIV-1 subtype C strains from antiretroviral therapy-naive subjects that display incomplete inhibition by maraviroc
K Borm, MR Jakobsen, K Cashin, JK Flynn, P Ellenberg, L Ostergaard, B Lee, MJ Churchill, M Roche, PR Gorry
Retrovirology | BIOMED CENTRAL LTD | Published : 2016
Abstract
Background: Entry of human immunodeficiency virus type 1 (HIV-1) into cells involves the interaction of the viral gp120 envelope glycoproteins (Env) with cellular CD4 and a secondary coreceptor, which is typically one of the chemokine receptors CCR5 or CXCR4. CCR5-using (R5) HIV-1 strains that display reduced sensitivity to CCR5 antagonists can use antagonist-bound CCR5 for entry. In this study, we investigated whether naturally occurring gp120 alterations in HIV-1 subtype C (C-HIV) variants exist in antiretroviral therapy (ART)-naïve subjects that may influence their sensitivity to the CCR5 antagonist maraviroc (MVC). Results: Using a longitudinal panel of 244 R5 Envs cloned from 20 ART-naï..
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Awarded by Australian Research Council
Funding Acknowledgements
We thank J. Sodroski for providing the pSVIII-Env plasmid controls used in this study, as well as pCMV Delta P1 Delta envpA and pHIV-1Luc plasmids. We also thank D. Mosier and R. Nedellec for supplying the NP2-CD4/CCR5 cells, and N. Shimizu and H. Hoshino for permission to use the NP2-CD4/CCR5 cells. Maraviroc was provided by Pfizer. This study was supported by a grant from the Australian National Health and Medical Research Council to PRG and MJC (APP1086178). KB is supported by a Victorian International Postgraduate Research Scholarship. JKF is supported by an RMIT Vice Chancellor's Postdoctoral Fellowship. KC and MR are supported by NHMRC Postdoctoral Training Fellowships. PRG was supported by an Australian Research Council (ARC) Future Fellowship. The authors gratefully acknowledge the contribution to this work of the Victorian Operational Infrastructure Support Program received by the Burnet Institute.