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

INTRODUCTION: The present study investigated the association between mannose-binding lectin (MBL) gene polymorphism and serum levels with infection by HIV-1. METHODS: Blood samples (5mL) were collected from 97 HIV-1-infected individuals resident in Belém, State of Pará, Brazil, who attended the Spec...

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Bibliographic Details
Published in:Revista da Sociedade Brasileira de Medicina Tropical
Main Authors: Antonio Carlos Rosário Vallinoto, Felipe Bonfim Freitas, Isabella Guirelli, Luiz Fernando Almeida Machado, Vânia Nakauth Azevedo, Izaura Cayres-Vallinoto, Marluísa Oliveira Guimarães Ishak, Ricardo Ishak
Format: Article in Journal/Newspaper
Language:English
Published: Sociedade Brasileira de Medicina Tropical (SBMT) 2011
Subjects:
HIV-1
Polimorfísmos no gene MBL
Região amazônica
Arctic medicine. Tropical medicine
RC955-962
Arctic
Ure
Online Access:https://doi.org/10.1590/S0037-86822011000100001
https://doaj.org/article/c9396d87fe9d49cf8df54aa469b5d764
Description
Summary:INTRODUCTION: The present study investigated the association between mannose-binding lectin (MBL) gene polymorphism and serum levels with infection by HIV-1. METHODS: Blood samples (5mL) 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. RESULTS: 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). CONCLUSIONS: 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.

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