Malaria in humans is caused by six species of Plasmodium parasites, of which the nuclear genome sequences for the two Plasmodium ovale spp., P. ovale curtisi and P. ovale wallikeri, and Plasmodium malariae have not yet been analyzed. Here we present an analysis of the nuclear genome sequences of these three parasites, and describe gene family expansions therein. Plasmodium ovale curtisi and P. ovale wallikeri are genetically distinct but morphologically indistinguishable and have sympatric ranges through the tropics of Africa, Asia and Oceania. Both P. ovale spp. show expansion of the surfin variant gene family, and an amplification of the Plasmodium interspersed repeat (pir) superfamily which results in an approximately 30% increase in genome size. For comparison, we have also analyzed the draft nuclear genome of P. malariae, a malaria parasite causing mild malaria symptoms with a quartan life cycle, long-term chronic infections, and wide geographic distribution. Plasmodium malariae shows only a moderate level of expansion of pir genes, and unique expansions of a highly diverged transmembrane protein family with over 550 members and the gamete P25/27 gene family. The observed diversity in the P. ovale wallikeri and P. ovale curtisi surface antigens, combined with their phylogenetic separation, supports consideration that the two parasites be given species status.
KAUST Repository Item: Exported on 2020-10-01
Acknowledgements: TJT was supported by a visiting professorship to the Institute of Tropical Medicine, Nagasaki University, Japan. JC was supported by grants from the National Natural Science Foundation of China (No. 81271870) and the National Natural Science Foundation of Jiangsu Province, China (No. BK20150001). AP is supported by faculty baseline funding from the King Abdullah University of Science and Technology (KAUST), Saudi Arabia and the Global Institute for Collaborative Research and Education (GI-CoRE) at the Center for Disease Control, Hokkaido University, Japan. RC is supported by Japanese Society of Parasitology (JSPS), Japan Grant-in-Aid for Scientific Research Nos. 24255009, 25870525 and 16K21233. MCO, EDB, TGC and CJS are supported by UK Medical Research Council Project Grant MR/L008661/1 to CJS. The authors thank the staff of the Bioscience Core Laboratory in KAUST for sequencing the DNA libraries. Osamu Kaneko is thanked for discussions and critical reading of the manuscript.
- Infectious Diseases