alexa Mannose-binding lectin variant associated with severe malaria in young African children.
General Science

General Science

Journal of Bioterrorism & Biodefense

Author(s): Holmberg V, Schuster F, Dietz E, Sagarriga Visconti JC, Anemana SD,

Abstract Share this page

Abstract Mannose-binding lectin (MBL) is a serum protein which initiates innate immune responses to microbial pathogens by binding to non-self surface oligosaccharides. MBL deficiency is the most common congenital immunodeficiency of human and has been shown to predispose to infections, particularly in children and immune compromised. In a matched case-control study among 870 Ghanaian children, we examined the influence of six polymorphisms of the MBL2 gene on Plasmodium falciparum infection and severe malaria. A missense mutation resulting in low MBL activity (MBL2*C) was found in 35\% of healthy controls, but in 42\% of asymptomatically infected children (P=0.01), and in 46\% of patients with severe malaria (P=0.007). Heterozygosity for MBL2*C was associated with increased odds of infection (odds ratio (OR), 1.6; 95\% confidence interval (CI), 1.1-2.1), severe malaria (OR, 1.7; 95\% CI, 1.2-2.4), and of severe anemia in particular (OR, 2.3; 95\% CI, 1.4-3.8). The population attributable fraction of severe malaria cases attributable to MBL2*C heterozygosity was 17\%. Our results suggest that the MBL pathway of the complement system is a critical determinant of both, susceptibility to P. falciparum infection and manifestation of severe malaria, particularly in young children in whom specific immune responses are weak or absent. This article was published in Microbes Infect and referenced in Journal of Bioterrorism & Biodefense

Relevant Expert PPTs

Relevant Speaker PPTs

Recommended Conferences

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

 
© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version
adwords