Influence of mannose-binding lectin gene polymorphisms on the invasiveness of cytomegalovirus disease after solid organ transplantation.

Published

Journal Article

BACKGROUND: Mannose-binding lectin (MBL) is a component of the innate immune system that binds the surface of pathogens, activating the complement pathway and acting as opsonin. Certain single-nucleotide polymorphisms of MBL2 are associated with a decrease in the circulating levels of MBL. Our aim was to evaluate the influence of MBL2 polymorphisms in the invasiveness of Cytomegalovirus (CMV) disease after solid organ transplantation. METHODS: We include those solid organ transplant recipients who developed CMV disease posttransplant from 2000 to 2006. MBL2 genotyping was performed by sequencing of exon 1 (wild-type allele A and variants B, C, and D) and promoter regions (alleles H and L, X and Y, and P and Q). In the case of liver transplantation, donor MBL2 genotypes were analyzed. Associations were calculated by the chi-square test and binary logistic regression. RESULTS: We included 45 transplant recipients with CMV disease (22 renal, 7 simultaneous kidney-pancreas, 11 liver, and 5 heart), of whom 10 (22%) had invasive CMV disease. No differences were found regarding HH (versus HL or LL), YY and YX (versus XX) and QQ (versus QP and PP) haplotypes with invasive CMV disease (P = 1.000 for all 3 comparisons). Patients with an exon 1 wild-type (AA) haplotype had 36% invasive CMV disease in comparison with 9% of patients with A/O or O/O haplotypes (P = .035). Binary logistic regression analysis showed that patients with exon 1 AA haplotype had an independent risk of developing invasive CMV disease (odds ratio, 6.0; 95% confidence interval, 1.1-32.5). CONCLUSIONS: Our results suggest that exon 1 wild-type genotypes are associated with a higher risk of invasive CMV disease after solid organ transplantation.

Full Text

Cited Authors

  • Cervera, C; Lozano, F; Linares, L; Antón, A; Balderramo, D; Suárez, B; Pascal, M; Sanclemente, G; Cofán, F; Ricart, MJ; Navasa, M; Roig, E; Marcos, MA; Pumarola, T; Moreno, A

Published Date

  • July 2009

Published In

Volume / Issue

  • 41 / 6

Start / End Page

  • 2259 - 2261

PubMed ID

  • 19715891

Pubmed Central ID

  • 19715891

Electronic International Standard Serial Number (EISSN)

  • 1873-2623

International Standard Serial Number (ISSN)

  • 0041-1345

Digital Object Identifier (DOI)

  • 10.1016/j.transproceed.2009.06.056

Language

  • eng