Rick M. Fairhurst, M.D., Ph.D.Twinbrook III, Room 3E10-A12735 Twinbrook ParkwayRockville, MD 20892-8132Phone: 301-402-7393Fax: email@example.com
Chief, Malaria Pathogenesis and Human Immunity Unit, LMVR
Research in the Malaria Pathogenesis and Human Immunity Unit focuses on three goals:
In each of the major areas of research, we seek discoveries that improve knowledge of malaria pathogenesis and protection and thereby support searches for new antimalarial therapeutics and vaccines. Research activities in our unit are integrated with field studies in malaria-endemic areas of Mali and Cambodia, where red blood cell polymorphisms are highly prevalent. Working in Cambodia enables us to study P. vivax malaria and artemisinin-resistant P. falciparum malaria, which are not present in Mali.
To read more about Dr. Fairhurst’s international work, read Fighting Drug-Resistant Malaria: Rick Fairhurst and Others at NIAID Go Global.
Inquiries about pre- and post-doctoral fellowships, as well as Ph.D. studentships in the NIH Graduate Partnership Program, are welcome.
Dr. Fairhurst received his M.D. and Ph.D. (molecular biology) degrees from the University of California, Los Angeles (UCLA). Following an internal medicine residency and an infectious diseases fellowship at UCLA Medical Center, he joined the Division of Intramural Research in 2001. As a clinical tenure-track investigator, Dr. Fairhurst focuses his laboratory’s work on elucidating the mechanisms of malaria pathogenesis, human genetic resistance to malaria, acquired immunity to malaria, and parasite resistance to the artemisinin class of antimalarial drugs. He travels frequently to malaria-endemic areas of Mali and Cambodia, where his trainees and colleagues enroll patients into clinical research protocols and use patient and parasite specimens in laboratory experiments. Presently, Dr. Fairhurst serves as president of the American Committee on Molecular, Cellular, and Immunoparasitology, a subcommittee of the American Society of Tropical Medicine and Hygiene. Recently, he was appointed deputy director of the National Institutes of Health M.D.-Ph.D. Partnership Training Program. In 2011, Dr. Fairhurst received the NIAID Outstanding Mentor of the Year Award.
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Lopera-Mesa TM, Mita-Mendoza NK, Doumbia S, Konaté D, Doumbouya M, van de Hoef D, Gu W, Traoré K, Diakité SAS, Remaley AT, Anderson JM, Rodriguez A, Fay MP, Long CA, Diakité M, Fairhurst RM. Plasma uric acid levels correlate with inflammation and disease severity in Malian children with Plasmodium falciparum malaria. PLoS One. 2012. In press.
Amaratunga C, Sreng S, Suon S, Phelps ES, Stepniewska K, Lim P, Zhou C, Mao S, Anderson JM, Lindegardh N, Jiang H, Song J, Su XZ, White NJ, Dondorp AM, Anderson TJC, Fay MP, Mu J, Duong S, Fairhurst RM. Artemisinin-resistant Plasmodium falciparum in Pursat province, western Cambodia: a parasite clearance rate study. Lancet Infect Dis. 2012 Aug 29. Epub ahead of print.
Fairhurst RM, Bess CD, Krause MA. Abnormal PfEMP1/knob display on Plasmodium falciparum-infected erythrocytes containing hemoglobin variants: fresh insights into malaria pathogenesis and protection. Microbes Infect. 2012 Aug 1;14(10):851-62.
Cholera R, Brittain NJ, Gillrie MR, Lopera-Mesa TM, Diakité SA, Arie T, Krause MA, Guindo A, Tubman A, Fujioka H, Diallo DA, Doumbo OK, Ho M, Wellems TE, Fairhurst RM. Impaired cytoadherence of Plasmodium falciparum-infected erythrocytes containing sickle hemoglobin. Proc Natl Acad Sci USA. 2008 Jan 22;105(3):991-6.
Guindo A, Fairhurst RM, Doumbo OK, Wellems TE, Diallo DA. X-linked G6PD deficiency protects hemizygous males but not heterozygous females against severe malaria. PLoS Med. 2007 Mar;4(3):e66.
Fairhurst RM, Baruch DI, Brittain NJ, Ostera GR, Wallach JS, Hoang HL, Hayton K, Guindo A, Makobongo MO, Schwartz OM, Tounkara A, Doumbo OK, Diallo DA, Fujioka H, Ho M, Wellems TE. Abnormal display of PfEMP-1 on erythrocytes carrying haemoglobin C may protect against malaria. Nature. 2005 Jun 23;435(7045):1117-21.
Visit PubMed for a complete publication listing.
In Mali, we just completed a 4-year longitudinal cohort study in which we diagnosed and treated 4,200 cases of P. falciparum malaria in 1,500 children. In this study, we aim to improve our understanding of how hemoglobin C, hemoglobin S, alpha-thalassemia, G6PD deficiency and blood group O antigen protect against malaria. We are also working to identify novel host immune and genetic factors that control the progression from uncomplicated to severe malaria. Presently, we are also working to identify host immune factors that influence parasite clearance rates in response to artemisinins.
In Cambodia, we recently completed longitudinal cohort and case-control studies in which we diagnosed and treated 2,000 cases of P. falciparum and P. vivax malaria. In these studies, we aim to improve our understanding of how hemoglobin E, alpha-thalassemia, G6PD deficiency, and blood group O antigen protect against severe P. falciparum malaria. We are also working to identify virulence determinants of P. vivax and host immune and genetic factors that control the progression from asymptomatic P. vivax parasitemia to symptomatic disease. More recently, we have studied parasite clearance rates in response to artemisinin in 500 patients from western, northern, and eastern Cambodia. Using data from all three sites, we aim to identify the P. falciparum genetic determinants of slow parasite clearance rates (‘artemisinin resistance’) in vivo.
Last Updated March 26, 2013