Frequency of CCR5 ∆32 Mutation in Human Immunodeficiency Virus (HIV)-seropositive and HIVexposed Seronegative Individuals and in General Population of Medellin, Colombia

ABSTRACT: Repeated exposure to human immunodeficiency virus (HIV) does not always result in seroconversion. Modifications in coreceptors for HIV entrance to target cells are one of the factors that block the infection. We studied the frequency of ∆32 mutation in ccr5 gene in Medellin, Colombia. Two...

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Autores:
Díaz Castrillón, Francisco Javier
Vega Parra, Jorge Arturo
Patiño Grajales, Pablo Javier
Vélez Rengifo, Gabriel Jaime
Nagles Pérez, Jorge Alberto
Villegas, Cecilia
Vesga Meneses, Rodrigo
Rugeles López, María Teresa
Tipo de recurso:
Article of investigation
Fecha de publicación:
2000
Institución:
Universidad de Antioquia
Repositorio:
Repositorio UdeA
Idioma:
eng
OAI Identifier:
oai:bibliotecadigital.udea.edu.co:10495/23664
Acceso en línea:
http://hdl.handle.net/10495/23664
Palabra clave:
Receptores CCR5
Receptores CCR5
HIV
VIH
∆32 mutation
Exposed seronegative
Rights
openAccess
License
http://creativecommons.org/licenses/by/2.5/co/
Description
Summary:ABSTRACT: Repeated exposure to human immunodeficiency virus (HIV) does not always result in seroconversion. Modifications in coreceptors for HIV entrance to target cells are one of the factors that block the infection. We studied the frequency of ∆32 mutation in ccr5 gene in Medellin, Colombia. Two hundred and eighteen individuals distributed in three different groups were analyzed for ∆32 mutation in ccr5 gene by polymerase chain reaction (PCR): 29 HIV seropositive (SP), 39 exposed seronegative (ESN) and 150 individuals as a general population sample (GPS). The frequency of the ∆32 mutant allele was 3.8% for ESN, 2.7% for GPS and 1.7% for SP. Only one homozygous mutant genotype (∆32/∆32) was found among the ESN (2.6%). The heterozygous genotype (ccr5/∆32) was found in eight GPS (5.3%), in one SP (3.4%) and in one ESN (2.6%). The differences in the allelic and genotypic frequencies among the three groups were not statistically significant. A comparison between the expected and the observed genotypic frequencies showed that these frequencies were significantly different for the ESN group, which indirectly suggests a protective effect of the mutant genotype (∆32/∆32). Since this mutant genotype explained the resistance of infection in only one of our ESN persons, different mechanisms of protection must be playing a more important role in this population.