Role of CCR5 genetic polymorphisms in clinical and histological outcomes of hepatitis C
Détails
ID Serval
serval:BIB_4A9F3DB3BA79
Type
Actes de conférence (partie): contribution originale à la littérature scientifique, publiée à l'occasion de conférences scientifiques, dans un ouvrage de compte-rendu (proceedings), ou dans l'édition spéciale d'un journal reconnu (conference proceedings).
Collection
Publications
Institution
Titre
Role of CCR5 genetic polymorphisms in clinical and histological outcomes of hepatitis C
Titre de la conférence
Annual Meeting of the Swiss Society of Gastroenterology, Swiss Society of Visceral Surgery, Swiss Association of the Study of the Liver and Swiss Society of Clinical Nutrition
Adresse
Interlaken, Switzerland, September 20-21, 2012
ISBN
1424-7860
ISSN-L
0036-7672
Statut éditorial
Publié
Date de publication
2012
Volume
142
Série
Swiss Medical Weekly
Pages
15S
Langue
anglais
Résumé
Background: The CCR5 32-base deletion (CCR5D32), which results
into the expression of a non-functioning receptor, has been associated
with H CV c learance a nd may influence fibrosis progression i n
hepatitis C . We a ssessed t he link between C CR5D32 and c linical
outcomes o f HCV. Methods: Genomic D NA was isolated and
analyzed b y PCR to i dentify C CR5D32 in 1 303 anti-HCV-positive
persons (161 clearers and 1142 chronically infected, 1007 with a liver
biopsy). Results: Overall, 200 (15.3%) w ere heterozygote a nd 16
(1.2%) homozygote for CCR5D32. H CV c learance (by univariate)
was associated with m ale sex (OR 0.633, 9 5% C I 0.428-0.935,
P=0.022), HCV acquisition by blood transfusion (OR 0.360, 95% CI
0.175-0.741, P =0.0056), polymorphisms at IL28B rs12979860 ( OR
0.482, 9 5% C I 0.277-0.839, P =0.0098) a nd rs8099917 ( OR 0.291,
95% CI 0.167-0.508, P=0.000014), but not with CCR5D32. However,
CCR5D32 was associated with spontaneous HCV clearance when the
482 females only w ere considered, although the number of
homozygotes was small (1/427 chronic vs 3/51 clearers) (OR 24.56,
95% C I 12.5-241.4, P =0.006). T he CCR5D32 deletion was not
associated with liver grading and staging scores, fibrosis progression
rate, or t herapy response. Conclusions: At v ariance w ith a p revious
report (Nattermann et a l, 2011), suggesting that a n on-functional
CCR5 m ay hamper H CV clearance, C CR5D32 appeared to b e
associated with an increased spontaneous eradication in women (but
not men). Given the small number of CCR5D32 homozygote persons,
these data need further validation.
into the expression of a non-functioning receptor, has been associated
with H CV c learance a nd may influence fibrosis progression i n
hepatitis C . We a ssessed t he link between C CR5D32 and c linical
outcomes o f HCV. Methods: Genomic D NA was isolated and
analyzed b y PCR to i dentify C CR5D32 in 1 303 anti-HCV-positive
persons (161 clearers and 1142 chronically infected, 1007 with a liver
biopsy). Results: Overall, 200 (15.3%) w ere heterozygote a nd 16
(1.2%) homozygote for CCR5D32. H CV c learance (by univariate)
was associated with m ale sex (OR 0.633, 9 5% C I 0.428-0.935,
P=0.022), HCV acquisition by blood transfusion (OR 0.360, 95% CI
0.175-0.741, P =0.0056), polymorphisms at IL28B rs12979860 ( OR
0.482, 9 5% C I 0.277-0.839, P =0.0098) a nd rs8099917 ( OR 0.291,
95% CI 0.167-0.508, P=0.000014), but not with CCR5D32. However,
CCR5D32 was associated with spontaneous HCV clearance when the
482 females only w ere considered, although the number of
homozygotes was small (1/427 chronic vs 3/51 clearers) (OR 24.56,
95% C I 12.5-241.4, P =0.006). T he CCR5D32 deletion was not
associated with liver grading and staging scores, fibrosis progression
rate, or t herapy response. Conclusions: At v ariance w ith a p revious
report (Nattermann et a l, 2011), suggesting that a n on-functional
CCR5 m ay hamper H CV clearance, C CR5D32 appeared to b e
associated with an increased spontaneous eradication in women (but
not men). Given the small number of CCR5D32 homozygote persons,
these data need further validation.
Création de la notice
14/02/2013 15:23
Dernière modification de la notice
20/08/2019 13:58
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