On the control of acute rodent malaria infections by innate immunity

• Published in: PloS one 2010-05, Vol.5 (5), p.e10444-e10444
• Main Authors: Kochin, Beth F, Yates, Andrew J, de Roode, Jacobus C, Antia, Rustom
• Format: Article
• Language: English
• Subjects: Analysis; Anemia; Animal models; Animals; Blood; Blood cells; Competition; Computational Biology; Control; Decay rate; Erythrocytes; Growth rate; Health aspects; Immune response; Immune system; Immunity; Immunity, Innate - immunology; Immunology/Innate Immunity; Infection; Infections; Infectious Diseases; Infectious Diseases/Protozoal Infections; Innate immunity; Malaria; Malaria - immunology; Malaria - parasitology; Malaria - prevention & control; Malaria - veterinary; Mathematical models; Mice; Models, Immunological; Parasite control; Parasites; Parasitology; Pathogens; Plasmodium chabaudi; Plasmodium chabaudi - immunology; Plasmodium yoelii; Rodents; Vector-borne diseases
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0010444

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.