Journal article

The magnitude of HIV-1 resistance to the CCR5 antagonist maraviroc may impart a differential alteration in HIV-1 tropism for macrophages and T-cell subsets

Jacqueline K Flynn, Geza Paukovics, Miranda S Moore, Anne Ellett, Lachlan R Gray, Renee Duncan, Hamid Salimi, Becky Jubb, Mike Westby, Damian FJ Purcell, Sharon R Lewin, Benhur Lee, Melissa J Churchill, Paul R Gorry, Michael Roche

Virology | ACADEMIC PRESS INC ELSEVIER SCIENCE | Published : 2013

Grants

Awarded by Australian National Health and Medical Research Council


Funding Acknowledgements

We thank J. Sodroski for providing pSVIII-YU-2 Env plasmid and for providing pCMV Delta P1 Delta envpA and pHIV-1Luc plasmids. We also thank D. Kabat for providing JC53 cells, N. Shimizu and H. Hoshino for permission to use NP2-CD4/CCR5 cells, and D. Mosier and R. Nedellec for supplying the NP2-CD4/CCR5 cells. We are also grateful to J. Mori and M. Lewis for their past contributions to this work, J. Demarest for helpful comments, and T. Spellman for advice with statistical analysis. Maraviroc was provided by Pfizer. This study was supported by a grant from the Australian National Health and Medical Research Council to PRG, MJC and SRL (1006534). PRG was the recipient of an Australian National Health and Medical Research Council (NHMRC) Level 2 Biomedical Career Development Award, and is now supported by an Australian Research Council (ARC) Future Fellowship (FT2). LRG is the recipient of an Australian NHMRC Postdoctoral Training Fellowship. HS is supported by a Postgraduate Research Scholarship from the Iranian Ministry of Health and Medical Education. SRL is the recipient of a NHMRC Practitioner Fellowship. The authors gratefully acknowledge the contribution to this work of the Victorian Operational Infrastructure Support Program received by the Burnet Institute. Pfizer assumes no responsibility for the validation and storage of the data shown in Figs. 1-4 and Table 2.