On the Control of Acute Rodent Malaria Infections by Innate Immunity

• Type of Material: Article
• Authors: Beth F. Kochin, Emory University; Andrew J. Yates, Albert Einstein College of Medicine; Jacobus De Roode, Emory University; Rustom Antia, Emory University
• Language: English
• Date: 2010
• Publisher: Public Library of Science
• Publication Version: Final Published Version
• Copyright Statement: © 2010 Kochin et al.
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0010444
• Title of Journal or Parent Work: PLoS ONE
• ISSN: 1932-6203
• Volume: 5
• Issue: 5
• Start Page: e10444
• End Page: e10444
• Grant/Funding Information: The National Institutes of Health (NIH grants U01-GM070749 and R01AI049334), the RAPIDD Program of the Fogarty Center, and the Fannie and John Hertz Foundation provided support.
• Research Categories: Health Sciences, Immunology; Health Sciences, General

Abstract

Does specific immunity, innate immunity or resource (red blood cell) limitation control the first peak of the blood-stage parasite in acute rodent malaria infections? Since mice deficient in specific immunity exhibit similar initial dynamics as wild-type mice it is generally viewed that the initial control of parasite is due to either limitation of resources (RBC) or innate immune responses. There are conflicting views on the roles of these two mechanisms as there is experimental evidence supporting both these hypotheses. While mathematical models based on RBC limitation are capable of describing the dynamics of primary infections, it was not clear whether a model incorporating the key features of innate immunity would be able to do the same. We examine the conditions under which a model incorporating parasite and innate immunity can describe data from acute Plasmodium chabaudi infections in mice. We find that innate immune response must decay slowly if the parasite density is to fall rather than equilibrate. Further, we show that within this framework the differences in the dynamics of two parasite strains are best ascribed to differences in susceptibility to innate immunity, rather than differences in the strains' growth rates or their propensity to elicit innate immunity. We suggest that further work is required to determine if innate immunity or resource limitation control acute malaria infections in mice.