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About the Authors:
Marika Orlov
Affiliations Seattle Biomedical Research Institute, Seattle, Washington, United States of America, Department of Medicine, University of California San Diego, La Jolla, California, United States of America
Florin Vaida
Affiliation: Department of Family and Preventive Medicine, University of California San Diego, La Jolla, California, United States of America
Olivia C. Finney
Affiliation: Seattle Biomedical Research Institute, Seattle, Washington, United States of America
David M. Smith
Affiliation: Department of Medicine, University of California San Diego, La Jolla, California, United States of America
Angela K. Talley
Affiliation: Seattle Biomedical Research Institute, Seattle, Washington, United States of America
Ruobing Wang
Affiliation: Seattle Biomedical Research Institute, Seattle, Washington, United States of America
Stefan H. Kappe
Affiliation: Seattle Biomedical Research Institute, Seattle, Washington, United States of America
Qianqian Deng
Affiliation: Department of Medicine, University of California San Diego, La Jolla, California, United States of America
Robert T. Schooley
* E-mail: [email protected]
Affiliation: Department of Medicine, University of California San Diego, La Jolla, California, United States of America
Patrick E. Duffy
Affiliations Seattle Biomedical Research Institute, Seattle, Washington, United States of America, Laboratory of Malaria Immunology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Rockville, Maryland, United States of America
Introduction
HIV-1 and Plasmodium falciparum malaria remain two of Sub-Saharan Africa’s major causes of morbidity and mortality. Together malaria and HIV caused nearly 2.5 million deaths in Africa during 2008. Although it was not initially fully appreciated [1], [2], increasing evidence indicates that the two pathogens interact in individuals and in populations. During acute bouts of clinical malaria, plasma HIV-1 RNA levels rise [3]–[5], and CD4 cells decline by approximately 40 cells/µL/year with each malaria episode [6] compared to the rate of decline in individuals without clinical malaria episodes. Conversely, in regions of unstable malaria transmission, HIV infection is associated with increased malaria disease severity and death [7]. Recently, a mathematical model further explored the potential importance of the malaria/HIV interaction. Based on this model, in an area of Kenya, with an adult population of roughly 200,000 that has been exposed to both pathogens since 1980, the interaction of the two diseases may have caused 8,500 excess HIV infections and 980,000 excess malaria episodes [8]. Supporting this mathematical model, a study that...