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Titolo:
THE ROLE OF A STROMAL CELL-DERIVED FACTOR-I CHEMOKINE GENE VARIANT INTHE CLINICAL COURSE OF HIV-1 INFECTION
Autore:
VANRIJ RP; BROERSEN S; GOUDSMIT J; COUTINHO RA; SCHUITEMAKER H;
Indirizzi:
NETHERLANDS RED CROSS,BLOOD TRANSFUS SERV,CENT LAB,DEPT CLIN VIROIMMUNOL,PLESMANLAAN 125 NL-1066 CX AMSTERDAM NETHERLANDS NETHERLANDS RED CROSS,BLOOD TRANSFUS SERV,CENT LAB,DEPT CLIN VIROIMMUNOL NL-1066 CX AMSTERDAM NETHERLANDS UNIV AMSTERDAM,ACAD MED CTR,EXPT & CLIN IMMUNOL LAB NL-1105 AZ AMSTERDAM NETHERLANDS UNIV AMSTERDAM,ACAD MED CTR,DEPT HUMAN RETROVIROL NL-1105 AZ AMSTERDAM NETHERLANDS MUNICIPAL HLTH SERV,DEPT PUBL HLTH & ENVIRONM AMSTERDAM NETHERLANDS
Titolo Testata:
AIDS
fascicolo: 9, volume: 12, anno: 1998,
pagine: 85 - 90
SICI:
0269-9370(1998)12:9<85:TROASC>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECEPTOR; ENTRY; IDENTIFICATION; MIP-1-ALPHA; LESTR/FUSIN; PROGRESSION; MIP-1-BETA; RANTES; LIGAND; SDF-1;
Keywords:
HIV-1; STROMAL CELL-DERIVED FACTOR-I; DISEASE PROGRESSION; KAPOSIS SARCOMA; VIRAL PHENOTYPE; CD4 T CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
23
Recensione:
Indirizzi per estratti:
Citazione:
R.P. Vanrij et al., "THE ROLE OF A STROMAL CELL-DERIVED FACTOR-I CHEMOKINE GENE VARIANT INTHE CLINICAL COURSE OF HIV-1 INFECTION", AIDS, 12(9), 1998, pp. 85-90

Abstract

Background: A G-to-A transition in the 3' untranslated region (UTR) of stromal cell-derived factor (SDF)-1 gene (SDF1-3'A) has recently been described, which in the homozygous state was associated with delayeddisease progression. Objective: To analyse the effect of the SDF-1 polymorphism on AIDS-free survival and survival after AIDS diagnosis, also in relation to viral phenotype. Design: Retrospective longitudinal study among 344 homosexual HIV-l-infected men. Results: A more rapid progression to AIDS (Centers for Disease Control and Prevention 1993 definition) was observed in SDF1-3'A,/3'A subjects than in wild-type (SDF1-wt/wt) subjects (relative hazard, 1.75; P = 0.07). Using death as an endpoint, accelerated progression was no longer observed (relative hazard, 0.93; P = 0.84), suggesting a late protective effect of the SDF1-3'A/3'A genotype. Indeed, survival after AIDS diagnosis was significantly delayed in SDF7-3'A/3'A subjects (relative hazard, 0.40; P = 0.02). No effect of the SDF1-3'A/wt genotype on disease progression was observed. Interestingly, a higher frequency of Kaposi's sarcoma was observed as the Al DS-defining event among SDF1-3'/3'A (40.0%) and SDF1-3'A/wt (30.6%) subjects than in SDF1-wt/wt subjects (17.0%). At the endof the study the total frequency of syncytium-inducing (SI) HIV-1 variants was lower in SDF7-3'A/3'A subjects (22.2%) than in SDF1-3'A/wt (32.5%) and SDF1-wt/wt subjects (40.5%), although not significantly. SDF-1 genotype did not influence the rate of evolution to SI HIV-1. Progression to AIDS after the emergence of SI HIV-1 was accelerated in SDF1-3'A/3'A subjects compared with the SDF1-wt/wt genotypic group (relative hazard, 4.04; P = 0.06). Conclusions: In our study group, homozygosity for a G-to-A transition in the 3' UTR of SDF-1 is associated withan accelerated progression to AIDS but a subsequent prolonged survival after AIDS diagnosis. (C) 1998 Lippincott-Raven Publishers.

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Documento generato il 04/12/20 alle ore 06:07:26