Sunil Parikh M.D., M.P.H.

Assistant Professor of Epidemiology (Microbial Diseases) and of Medicine (Infectious Diseases)

Research Interests

Translation research in malaria; Pharmacology of antimalarials; HIV-malaria co-infection; Host response to malaria infection; Innate immunity to malaria

Current Projects

1) Antimalarial Therapy in the context of pregnancy, growth/development, and HIV coinfection in Uganda

Major Goal: To assess the pharmacokinetics and pharmacodynamics of artemisinin-combination therapies and their impact upon efficacy and drug resistance in vulnerable populations

2) Innate Immune Responses in Populations with Differing Susceptibility to Malaria in Burkina Faso

Major Goal: Through the study of early transcriptional and functional cellular responses in two ethnic groups with differing susceptibility to malaria, we will identify the key innate pathways which underlie this differential ability to control parasitemia

3) Antimalarial-Antiretroviral Drug Interaction studies in Nigeria, Tanzania, and Malawi

4) Dynamic Malaria Modelling in conjunction with the Galvani group


Research Summary

Professor Parikh’s research interests focus on translational studies of malaria in sub-Saharan Africa. Dr. Parikh focuses upon several aspects of malaria: early host immune responses to infection, human genetics, and treatment. Current projects include: (1) understanding host factors affecting response to artemisinin-based antimalarial therapies using a combination of individual and population-based pharmacologic approaches to inform treatment guidelines; 2) characterizing the impact of host genetic and transcriptional variability in early immune responses to malaria; and 3) understanding the impact of the HIV epidemic on the treatment of malaria in co-endemic regions. Dr. Parikh has ongoing projects in several African countries, including Uganda, Burkina Faso, and Nigeria.


Selected Publications

  • Gong L, Parikh S, Rosenthal PJ, Greenhouse B. Biochemical and immunological mechanisms by which sickle cell trait protects against malaria. Malar J. 2013 Sep 11;12(1):317.
  • Creek DJ, Bigira V, McCormack S, Arinaitwe E, Wanzira H, Kakuru A, Tappero JW, Sandison TG, Lindegardh N, Nosten F, Aweeka FT, Parikh S. Pharmacokinetic predictors for recurrent malaria after dihydroartemisinin-piperaquine treatment of uncomplicated malaria in Ugandan infants. The Journal of Infectious Diseases. 2013 Jun 1;207(11):1646-54
  • Tarning J, Zongo I, Some F, Romba N , Parikh S, et al. Population pharmacokinetics and pharmacodynamics of piperaquine in children with uncomplicated falciparum malaria. Clinical Pharmacology and Therapeutics 2012; 91(3):497-505.
  • Kim CC, Parikh S, Sun JC, Myrick A, Lanier LL, Rosenthal PJ, DeRisi JL. Experimental Malaria Infection Triggers Early Expansion of Natural Killer Cells. Infection and Immunity 2008; 76(12): 5873-5872
  • Lee TM, Huang L, Johnson MK, Lizak P, Kroetz D, Aweeka F, Parikh S. In vitro metabolism of piperaquine is primarily mediated by CYP3A4. Xenobiotica. 2012: 42(11): 1088-95. PMID: 22671777.
  • Mwesigwa J*, Parikh S*, Clark T, Njama-Meya D, Rosenthal P, Aweeka F. “Pharmacokinetics of artemisinin-combination therapies in Ugandan children”, Antimicrobial Agents and Chemotherapy 2009; 54(1):52-9.
  • Johnson MK, Dorsey G, Clark TD, Roenthal PJ, Parikh S. Impact of the method of G6PD deficiency assessment in genetic association studies of malaria susceptibility. PLoS One 2009; 4(9): e7246
  • 5. Parikh S, Quedraogo JB, Goldstien JA, Rosenthal PJ, Kroetz DL. Amodiaquine metabolism is impaired by common polymorphisms in CYP2C8: Implications. for malaria treatment in Africa. Clinical Pharmacology and Therapeutics 2007; 82(2): 197-203
  • Parikh S, Gut J, Istvan E, Goldberg DJ, Havlir D, Rosenthal PJ. Antimalarial activity of HIV-1 protease inhibitors. Antimicrobial Agents and Chemotherapy 2005; 49(7): 2983-2985.

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