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Nicolas Sluis-Cremer, PhD

Dr. Nicolas Sluis-Cremer


Fax: 412-648-8521
S817 Scaife Hall
3550 Terrace Street


Postdoctoral, McGill University AIDS Center, Canada

PhD, University of the Witwatersrand, South Africa

BSc (Honors), University of the Witwatersrand, South Africa

BSc, University of the Witwatersrand, South Africa

Academic Affiliation(s)

Associate Professor, Department of Medicine, Division of Infectious Diseases

Associate Professor, Department of Microbiology and Molecular Genetics

Associate Professor, Graduate School of Public Health, Department of Infectious Diseases and Microbiology

Member, Molecular Virology and Microbiology Graduate Program


Dr Sluis-Cremer's research focuses on antiretroviral drugs, drug resistance and HIV latency. Projects include understanding the biochemistry and cellular biology of HIV reverse transcription, elucidating the mechanisms of action and resistance to HIV antiviral drugs, and the discovery of novel inhibitors active against drug resistant HIV-1. New initiatives include understanding the mechanisms involved in HIV latency and pharmacological approaches to eradicate latent HIV infection.

Lab Personnel

Kelly Huber, Research Specialist IV
Genevieve Doyon, Postdoctoral Fellow
Brian Herman, Postdoctoral Fellow
Jennifer Zerbato, Graduate Student

Areas of Interest

HIV; drug discovery; drug resistance; latency; persistence


Herman B. D, Schinazi R. F, Zhang H. W, Nettles J. H, Stanton R, Detorio M, Obikhod A, Pradere U, Coats S. J, Mellors J. W, and Sluis-Cremer N. Substrate mimicry: HIV-1 reverse transcriptase recognizes 6-modified-3'-azido-2',3'-dideoxyguanosine-5'-triphosphates as adenosine analogs. Nucleic Acids Res. 40: 381-390. |  View Abstract

Doyon G, Zerbato J, Mellors J. W, and Sluis-Cremer N. Disulfiram reactivates latent HIV-1 expression through depletion of the phosphatase and tensin homolog (PTEN). AIDS. [epub ahead of print 6/29/12] |  View Abstract

Brehm J. H, Scott Y, Koontz D. L, Perry S, Hammer S, Katzenstein D, Mellors J. W, Sluis-Cremer N. Zidovudine (AZT) monotherapy selects for the A360V mutation in the connection domain of HIV-1 reverse transcriptase. PLoS One. 7: e31558. |  View Abstract

Huber, K, Doyon G, Plaks J, Fyne E, Mellors J. W, and Sluis-Cremer N. Inhibitors of histone deacetylases: correlation between isoform specificity and reactivation of HIV type 1 (HIV-1) from latently infected cells. J Biol Chem. 286: 22211-22218. |  View Abstract

Sluis-Cremer N, Moore K, Radzio J, Sonza S, and Tachedjian G. N348I in HIV-1 reverse transcriptase decreases susceptibility to tenofovir and etravirine in combination with other resistance mutations. Aids. 24: 317-319. |  View Abstract

Radzio J, Yap S. H, Tachedjian G, and Sluis-Cremer N. N348I in reverse transcriptase provides a genetic pathway for HIV-1 to select thymidine analogue mutations and mutations antagonistic to thymidine analogue mutations. Aids. 24: 659-667. |  View Abstract

Sluis-Cremer N, Koontz D, Bassit L, Hernandez-Santiago B. I, Detorio M, Rapp K. L, Amblard F, Bondada L, Grier J, Coats S. J, Schinazi R. F, and Mellors J. W. Anti-human immunodeficiency virus activity, cross-resistance, cytotoxicity, and intracellular pharmacology of the 3'-azido-2',3'-dideoxypurine nucleosides. Antimicrob Agents Chemother. 53: 3715-3719. |  View Abstract