In:
Liver International, Wiley, Vol. 36, No. 9 ( 2016-09), p. 1267-1274
Kurzfassung:
Infectious hepatitis C virus (HCV) particles bind to host lipoproteins such as low‐density lipoproteins ( LDLs ). Low‐density lipoprotein receptors (LDLR) have been termed candidate receptors for HCV – LDL complexes. Functional host genetic single nucleotide polymorphisms ( SNP s) in the apolipoprotein E ( APOE ) gene encoding apolipoprotein E (apoE) – a major structural LDL component and natural ligand of LDLR – likely influence the course of HCV infection. We investigated the prevalence of APOE SNP s in two large and independent cohorts of patients with chronic HCV infection compared to respective controls. Methods We genotyped 996 chronically HCV ‐infected patients; 179 patients with spontaneous HCV clearance; 283 individuals with non‐ HCV ‐associated liver disease; and 2 234 healthy controls. Results APOE genotype proportions in patients with persistent HCV infection significantly differed from healthy controls ( P = 0.007) primarily because of a substantial under‐representation of APOE 4 alleles in chronically HCV ‐infected patients (10.2%) compared to 13.0% in healthy controls ( P = 0.001). The distribution of APOE 4 allele positive genotypes (ε2ε4, ε3ε4, ε4ε4) also significantly differed between chronically HCV ‐infected patients and healthy controls (1.4%, 17%, 1% vs. 2.4%, 20.5%, 1.7%; P = 0.001), suggesting a protective effect of the APOE 4 allele in HCV infection. This was confirmed by a significant over‐representation of the APOE 4 allele in patients with spontaneous HCV clearance (17.6%; P = 0.00008). The APOE 4 allele distribution in patients with non‐ HCV ‐associated liver disease (14.0%) was very similar to healthy controls and also differed from chronically HCV ‐infected patients ( P = 0.012), suggesting HCV specificity. Conclusions Our findings suggest that the APOE 4 allele may confer a protective effect in the course of HCV infection.
Materialart:
Online-Ressource
ISSN:
1478-3223
,
1478-3231
DOI:
10.1111/liv.2016.36.issue-9
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2016
ZDB Id:
2124684-1
