Malaria-driven adaptation of MHC class I in wild bonobo populations

Emily E. Wroblewski, Lisbeth A. Guethlein, Aaron G. Anderson, Weimin Liu, Yingying Li, Sara E. Heisel, Andrew Jesse Connell, Jean-Bosco N. Ndjango, Paco Bertolani, John A. Hart, Terese B. Hart, Crickette M. Sanz, David B. Morgan, Martine Peeters, Paul M. Sharp, Beatrice H. Hahn, Peter Parham

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

The malaria parasite Plasmodium falciparum causes substantial human mortality, primarily in equatorial Africa. Enriched in affected African populations, the B*53 variant of HLA-B, a cell surface protein that presents peptide antigens to cytotoxic lymphocytes, confers protection against severe malaria. Gorilla, chimpanzee, and bonobo are humans’ closest living relatives. These African apes have HLA-B orthologs and are infected by parasites in the same subgenus (Laverania) as P. falciparum, but the consequences of these infections are unclear. Laverania parasites infect bonobos (Pan paniscus) at only one (TL2) of many sites sampled across their range. TL2 spans the Lomami River and has genetically divergent subpopulations of bonobos on each side. Papa-B, the bonobo ortholog of HLA-B, includes variants having a B*53-like (B07) peptide-binding supertype profile. Here we show that B07 Papa-B occur at high frequency in TL2 bonobos and that malaria appears to have independently selected for different B07 alleles in the two subpopulations.
Original languageEnglish
Article number1033
Number of pages11
JournalNature Communications
Issue number1
Early online date23 Feb 2023
Publication statusPublished - 23 Feb 2023


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