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Mamm Genome. 2018 Aug;29(7-8):488-506. doi: 10.1007/s00335-018-9752-9. Epub 2018 Jun 19.

Genetic analysis of cerebral malaria in the mouse model infected with Plasmodium berghei.

Author information

1
Department of Biochemistry, Department of Human Genetics, McGill University Research Centre on Complex Traits, McGill University, Montreal, QC, Canada.
2
McGill University and Genome Quebec Innovation Centre, Montreal, QC, Canada.
3
Department of Biochemistry, Department of Human Genetics, McGill University Research Centre on Complex Traits, McGill University, Montreal, QC, Canada. philippe.gros@mcgill.cag.
4
Department of Biochemistry, McGill University, 3649 Sir William Osler Promenade, room 366, Montreal, QC, H3G-0B1, Canada. philippe.gros@mcgill.cag.

Abstract

Malaria is a common and sometimes fatal disease caused by infection with Plasmodium parasites. Cerebral malaria (CM) is a most severe complication of infection with Plasmodium falciparum parasites which features a complex immunopathology that includes a prominent neuroinflammation. The experimental mouse model of cerebral malaria (ECM) induced by infection with Plasmodium berghei ANKA has been used abundantly to study the role of single genes, proteins and pathways in the pathogenesis of CM, including a possible contribution to neuroinflammation. In this review, we discuss the Plasmodium berghei ANKA infection model to study human CM, and we provide a summary of all host genetic effects (mapped loci, single genes) whose role in CM pathogenesis has been assessed in this model. Taken together, the reviewed studies document the many aspects of the immune system that are required for pathological inflammation in ECM, but also identify novel avenues for potential therapeutic intervention in CM and in diseases which feature neuroinflammation.

PMID:
29922917
DOI:
10.1007/s00335-018-9752-9
[Indexed for MEDLINE]

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