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Short report: codon 125 polymorphism of CD31 and susceptibility to malaria

C Casals-Pascual1, S Allen, A Allen

  • 1Nuffield Department of Clinical Laboratory Sciences and National Blood Service, John Radcliffe Hospital, Headington, Oxford, United Kingdom.

The American Journal of Tropical Medicine and Hygiene
|January 17, 2002
PubMed

Insights

A common genetic variation in Platelet-endothelial cell adhesion molecule 1 (PECAM-1/CD31) does not protect against severe malaria. This finding suggests other factors influence this genetic polymorphism in malaria-endemic regions.

Area of Science:

  • Immunology
  • Genetics
  • Infectious Diseases

Background:

  • Platelet-endothelial cell adhesion molecule 1 (PECAM-1/CD31) is an endothelial cell receptor for Plasmodium falciparum-infected erythrocytes.
  • The role of infected erythrocyte adhesion to PECAM-1/CD31 in malaria pathogenesis remains unclear.

Purpose of the Study:

  • To investigate the association between a specific PECAM-1/CD31 gene mutation (codon 125 CTG-->GTG) and severe malaria.
  • To determine if this functional polymorphism confers protection against severe malaria outcomes.

Main Methods:

  • Two case-control studies were conducted in malaria-affected regions: Madang Hospital, Papua New Guinea, and Kilifi District Hospital, Kenya.
  • Genotyping for the codon 125 polymorphism in the Cd31 gene was performed on 442 cases and controls from Papua New Guinea and 396 cases and controls from Kenya.

Main Results:

  • The codon 125 polymorphism in the Cd31 gene was not significantly associated with severe malaria in either the Papua New Guinea or Kenyan study populations.
  • No evidence suggests that the Leu-->Val substitution at codon 125 of CD31 provides protection against severe malaria.

Conclusions:

  • The CTG-->GTG (Leu-->Val) substitution at codon 125 in CD31 is not linked to protection from severe malaria.
  • High-frequency maintenance of this PECAM-1/CD31 polymorphism is likely driven by selective pressures unrelated to malaria resistance.

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