Characterization of mannose-binding lectin plasma levels and genetic polymorphisms in HIV-1-infected individuals

• Published in: Revista da Sociedade Brasileira de Medicina Tropical 2011-01, Vol.44 (1), p.1-3
• Main Authors: Vallinoto, Antonio Carlos Rosário, Freitas, Felipe Bonfim, Guirelli, Isabella, Machado, Luiz Fernando Almeida, Azevedo, Vânia Nakauth, Cayres-Vallinoto, Izaura, Ishak, Marluísa Oliveira Guimarães, Ishak, Ricardo
• Format: Article
• Language: English
• Subjects: Adult; Case-Control Studies; CD4 Lymphocyte Count; HIV Infections - blood; HIV Infections - genetics; HIV Infections - virology; HIV-1; HIV-1 - genetics; Humans; Mannose-Binding Lectin - blood; Mannose-Binding Lectin - genetics; Polimorfísmos no gene MBL; Polymerase Chain Reaction; Polymorphism, Genetic - genetics; Região amazônica; TROPICAL MEDICINE; Viral Load
• ISSN: 0037-8682; 1678-9849; 1678-9849; 0037-8682
• DOI: 10.1590/S0037-86822011000100001

The present study investigated the association between mannose-binding lectin (MBL) gene polymorphism and serum levels with infection by HIV-1. Blood samples (5 mL) were collected from 97 HIV-1-infected individuals resident in Belém, State of Pará, Brazil, who attended the Special Outpatient Unit for Infections and Parasitic Diseases (URE-DIPE). CD4+ T-lymphocyte count and plasma viral load were quantified. A 349bp fragment of exon 1 of the MBL was amplified via PCR, using genomic DNA extracted from controls and HIV-1-infected individuals, following established protocols. MBL plasma levels of the patients were quantified using an enzyme immunoassay kit. Two alleles were observed: MBL*O, with a frequency of 26.3% in HIV-1-infected individuals; and the wild allele MBL*A (73.7%). Similar frequencies were observed in the control group (p > 0.05). Genotype frequencies were distributed according to the Hardy-Weinberg equilibrium in both groups. Mean MBL plasma levels varied by genotype, with statistically significant differences between the AA and AO (p < 0.0001), and AA and OO (p < 0.001) genotypes, but not AO and OO (p = 0.17). Additionally, CD4+ T-lymphocytes and plasma viral load levels did not differ significantly by genotype (p > 0.05). The results of this study do not support the hypothesis that MBL gene polymorphism or low plasma MBL concentrations might have a direct influence on HIV-1 infection, although a broader study involving a large number of patients is needed.