Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/48638
Título: Influence of mannose-binding lectin on HIV infection and tuberculosis in a Western-European population
Autores/as: Garcia-Laorden, M. Isabel
Pena, M. Jose
Caminero Luna, José Antonio 
Garcia-Saavedra, Ayoze
Campos-Herrero, M. Isolina 
Caballero, Araceli
Rodriguez-Gallego, Carlos 
Clasificación UNESCO: 32 Ciencias médicas
2302 Bioquímica
Palabras clave: Tuberculosis
HIV
Genotype
Fecha de publicación: 2006
Publicación seriada: Molecular Immunology 
Resumen: Mannose-binding lectin (MBL) is a serum lectin that mediates phagocytosis and activates complement. Its deficiency has been associated with increased susceptibility to infectious diseases, mainly in childhood. However, non-producer mbl-2 alleles are common in most populations, suggesting a selective advantage of these alleles. We have analysed the association of mbl-2 structural and promoter polymorphisms with HIV infection and tuberculosis (TBC) in a white Spanish population, including 615 HIV patients with and without TBC, 127 no-HIV TBC patients, 142 TBC household contacts and 344 controls. The frequency of low or non-producer mbl-2 genotypes was lower in HIV patients than in controls. HIV-TBC patients presented lower frequencies of low or non-producer alleles and genotypes than HIV no-TBC patients and controls. Additionally, we found a significantly positive correlation between the incidence of TBC and the frequency of non-producer mbl-2 alleles in Western Europe. Therefore, MBL deficiency may be associated with a lower risk of HIV infection, and also of active TBC, at least in HIV patients. The protective role of low-producer mbl-2 genotypes against TBC together with the positive correlation observed between non-producer mbl-2 alleles and TBC incidence, suggest a balancing selection: in spite of an increased susceptibility to respiratory infections associated with MBL deficiency, mbl-2 deficient alleles would have been selected along different populations as a consequence of its selective advantage against intracellular pathogens, such as M. tuberculosis.
URI: http://hdl.handle.net/10553/48638
ISSN: 0161-5890
DOI: 10.1016/j.molimm.2006.01.008
Fuente: Molecular Immunology[ISSN 0161-5890],v. 43, p. 2143-2150 (Julio 2006)
Colección:Artículos
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