TY - JOUR
T1 - Homozygous Δ32 deletion of the CCR-5 chemokine receptor gene in an HIV-1-infected patient
AU - Balotta, Claudia
AU - Bagnarelli, Patrizia
AU - Violin, Michela
AU - Ridolfo, Anna Lisa
AU - Zhou, Dan
AU - Berlusconi, Alberto
AU - Corvasce, Stefano
AU - Corbellino, Mario
AU - Clementi, Massimo
AU - Clerici, Mario
AU - Moroni, Mauro
AU - Galli, Massimo
PY - 1997
Y1 - 1997
N2 - Background: Recent research has found that entry of non-syncytium-inducing (NSI),monocyte-macrophage-tropic HIV-1 isolates requires binding to both CD4 and CCR5 receptors, and that Δ32/Δ32 homozygous individuals are protected against infection. Objective: To analyse the polymorphism of CCR-5 gene in HIV-1-infected and uninfected subjects. Design and methods: CCR-5 sequences were amplified by polymerase chain reaction (PCR) from DNA of peripheral blood mononuclear cells. Samples from 152 HIV-1-infected subjects and 122 uninfected controls were tested for the detection of the 32 base-pair deletion. HIV-1 phenotype was determined by viral isolation and MT-2 evaluation. Results: The wild-type/Δ32 heterozygous and Δ32/Δ32 homozygous conditions were represented in 10.7 and 0.8% of healthy controls and in 9.8 and 0.7% of HIV-1-infected subjects, respectively. Of note, the Δ32/Δ32 deletion of the CCR-5 gene was detected by PCR and sequencing confirmed in a patient with progressive infection harbouring a clade B virus with SI phenotype. Conclusions: Δ32/Δ32 homozygosity for the CCR-5 gene does not confer absolute protection against HIV-1 infection, suggesting that either macrophage-tropic viral strains could use coreceptors other than CCR-5 or infect independently of the presence of a functional CCR-5 coreceptor. Alternatively, primary infection sustained by T-cell-tropic isolates, although exceptional, may occur.
AB - Background: Recent research has found that entry of non-syncytium-inducing (NSI),monocyte-macrophage-tropic HIV-1 isolates requires binding to both CD4 and CCR5 receptors, and that Δ32/Δ32 homozygous individuals are protected against infection. Objective: To analyse the polymorphism of CCR-5 gene in HIV-1-infected and uninfected subjects. Design and methods: CCR-5 sequences were amplified by polymerase chain reaction (PCR) from DNA of peripheral blood mononuclear cells. Samples from 152 HIV-1-infected subjects and 122 uninfected controls were tested for the detection of the 32 base-pair deletion. HIV-1 phenotype was determined by viral isolation and MT-2 evaluation. Results: The wild-type/Δ32 heterozygous and Δ32/Δ32 homozygous conditions were represented in 10.7 and 0.8% of healthy controls and in 9.8 and 0.7% of HIV-1-infected subjects, respectively. Of note, the Δ32/Δ32 deletion of the CCR-5 gene was detected by PCR and sequencing confirmed in a patient with progressive infection harbouring a clade B virus with SI phenotype. Conclusions: Δ32/Δ32 homozygosity for the CCR-5 gene does not confer absolute protection against HIV-1 infection, suggesting that either macrophage-tropic viral strains could use coreceptors other than CCR-5 or infect independently of the presence of a functional CCR-5 coreceptor. Alternatively, primary infection sustained by T-cell-tropic isolates, although exceptional, may occur.
KW - Δ32/Δ32 deletion
KW - CCR-5 gene
KW - HIV-1 non-syncytium-inducing/macrophage-tropic isolates
KW - HIV-1 syncytium-inducing/T-cell-tropic isolates
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U2 - 10.1097/00002030-199710000-00001
DO - 10.1097/00002030-199710000-00001
M3 - Article
C2 - 9256936
AN - SCOPUS:8544234244
VL - 11
JO - AIDS
JF - AIDS
SN - 0269-9370
IS - 10
ER -