Antibody-independent mechanisms regulate the establishment of chronic Plasmodium infection

作者：Brugat Thibaut^*; Reid Adam James^*; Lin Jing wen; Cunningham Deirdre; Tumwine Irene; Kushinga Garikai; McLaughlin Sarah; Spence Philip; Boehme Ulrike; Sanders Mandy; Conteh Solomon; Bushell Ellen; Metcalf Tom; Billker Oliver; Duffy Patrick E; Newbold Chris; Berriman Matthew; Langhorne Jean

来源：Nature Microbiology, 2017, 2(4): 16276.

DOI：10.1038/nmicrobiol.2016.276

Malaria is caused by parasites of the genus Plasmodium. All human-infecting Plasmodium species can establish longlasting chronic infections(1-5), creating an infectious reservoir to sustain transmission(1),(6). It is widely accepted that the maintenance of chronic infection involves evasion of adaptive immunity by antigenic variation(7). However, genes involved in this process have been identified in only two of five human-infecting species: Plasmodium falciparum and Plasmodium knowlesi. Furthermore, little is understood about the early events in the establishment of chronic infection in these species. Using a rodent model we demonstrate that from the infecting population, only a minority of parasites, expressing one of several clusters of virulence- associated pir genes, establishes a chronic infection. This process occurs in different species of parasites and in different hosts. Establishment of chronicity is independent of adaptive immunity and therefore different from the mechanism proposed for maintenance of chronic P. falciparum infections(7)- . Furthermore, we show that the proportions of parasites expressing different types of pir genes regulate the time taken to establish a chronic infection. Because pir genes are common to most, if not all, species of Plasmodium(10,) this process may be a common way of regulating the establishment of chronic infections.

• 出版日期2017-4
• 单位河北医科大学