Evidence for malaria selection of a CR1 haplotype in Sardinia

R. Kosoy, M. Ransom, H. Chen, M. Marconi, F. MacCiardi, N. Glorioso, P. K. Gregersen, D. Cusi, Michael F Seldin

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

Complement receptor 1 (CR1) levels have been associated with malarial susceptibility and/or severity of the disease in different population groups, and CR1 is a receptor for Plasmodium falciparum. In this study, multiple CR1 single-nucleotide polymorphisms (SNPs) showed strong evidence of population differentiation between Sardinian and other European ethnic groups. Cross population algorithms comparing haplotype structure and differences in haplotype and allele frequency distribution provided additional support for natural selection of CR1 in Sardinia. The predominant Sardinian CR1 haplotype included SNPs that are associated with decreased CR1 levels in Europeans and other population groups. Previous studies have shown that the SNPs within the dominant Sardinian haplotype have a significantly higher frequency in a malaria endemic compared with non-endemic regions in India. Together with the historical evidence of the prevalence of malaria in Sardinia, these data support the role of malaria leading to positive selection of this CR1 haplotype in Sardinia.

Original languageEnglish (US)
Pages (from-to)582-588
Number of pages7
JournalGenes and Immunity
Volume12
Issue number7
DOIs
StatePublished - Oct 20 2011

Keywords

  • CR1
  • malaria, natural selection
  • population differentiation
  • Sardinia

ASJC Scopus subject areas

  • Genetics(clinical)
  • Immunology
  • Genetics

Fingerprint Dive into the research topics of 'Evidence for malaria selection of a CR1 haplotype in Sardinia'. Together they form a unique fingerprint.

  • Cite this

    Kosoy, R., Ransom, M., Chen, H., Marconi, M., MacCiardi, F., Glorioso, N., Gregersen, P. K., Cusi, D., & Seldin, M. F. (2011). Evidence for malaria selection of a CR1 haplotype in Sardinia. Genes and Immunity, 12(7), 582-588. https://doi.org/10.1038/gene.2011.33