title: Influence of mannose-binding lectin gene polymorphisms on the invasiveness of cytomegalovirus disease after solid organ transplantation.
abstract: 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.
authors.affiliation: Infectious Diseases Service, Hospital Clinic, IDIBAPS, University of Barcelona, Barcelona, Spain. ccervera@clinic.ub.es
authors.forename: C
authors.initials: C
authors.lastname: Cervera
authors.forename: F
authors.initials: F
authors.lastname: Lozano
authors.forename: L
authors.initials: L
authors.lastname: Linares
authors.forename: A
authors.initials: A
authors.lastname: Antón
authors.forename: D
authors.initials: D
authors.lastname: Balderramo
authors.forename: B
authors.initials: B
authors.lastname: Suárez
authors.forename: M
authors.initials: M
authors.lastname: Pascal
authors.forename: G
authors.initials: G
authors.lastname: Sanclemente
authors.forename: F
authors.initials: F
authors.lastname: Cofán
authors.forename: M J
authors.initials: MJ
authors.lastname: Ricart
authors.forename: M
authors.initials: M
authors.lastname: Navasa
authors.forename: E
authors.initials: E
authors.lastname: Roig
authors.forename: M A
authors.initials: MA
authors.lastname: Marcos
authors.forename: T
authors.initials: T
authors.lastname: Pumarola
authors.forename: A
authors.initials: A
authors.lastname: Moreno
mesh_terms: D003586:Cytomegalovirus Infections / Q000453:epidemiology / Q000235:genetics*; D005091:Exons / Q000235:genetics*; D005260:Female; D005838:Genotype; D006239:Haplotypes / Q000235:genetics; D016027:Heart Transplantation / Q000009:adverse effects*; D006801:Humans; D016030:Kidney Transplantation / Q000009:adverse effects*; D016031:Liver Transplantation / Q000009:adverse effects*; D008297:Male; D037601:Mannose-Binding Lectin / Q000097:blood / Q000172:deficiency / Q000235:genetics*; D016035:Pancreas Transplantation / Q000009:adverse effects*; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic; D012720:Severity of Illness Index
chemical_list: C445619:MBL2 protein, human; D037601:Mannose-Binding Lectin