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Nat Microbiol. 2017 Feb 6;2:16276. doi: 10.1038/nmicrobiol.2016.276.

Antibody-independent mechanisms regulate the establishment of chronic Plasmodium infection.

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  • 1The Francis Crick institute, London NW1 1AT, UK.
  • 2Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK.
  • 3MRC National Institute for Medical Research, London NW7 1AA, UK.
  • 4Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA.
  • 5Weatherall Institute of Molecular Medicine, Oxford OX3 9DS, UK.


Malaria is caused by parasites of the genus Plasmodium. All human-infecting Plasmodium species can establish long-lasting chronic infections1-5, creating an infectious reservoir to sustain transmission1,6. It is widely accepted that the maintenance of chronic infection involves evasion of adaptive immunity by antigenic variation7. 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 infections7-9. 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 Plasmodium10, this process may be a common way of regulating the establishment of chronic infections.

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