IL28B: Relevance extended to hepatitis B virus or limited to interferon-based therapies in hepatitis C virus?
Journal
Liver International
Journal Volume
31
Journal Issue
8
Pages
1068-1070
Date Issued
2011
Author(s)
Tillmann H.L.
Abstract
The three top single-nucleotide polymorphism (SNPs) rs12979860, rs12980275 and rs8099917 were recently related to treatment-induced hepatitis C virus (HCV) clearance. Thio and Thomas (1) elegantly reviewed that rs8099917 is likely irrelevant in the setting of African American patients. Furthermore, several studies confirmed that rs12979860 seems to be the most dominant SNP in Caucasian populations (2). In contrast, in an Asian population, rs8099917 has been superior to rs12979860 for predicting HCV treatment response or spontaneous clearance in some (3, 4) but not all studies (5). Shortly after the discovery of the Type III or interferon (IFN)-λ, it was shown that these IFNs can inhibit HCV and hepatitis B virus (HBV) replication. However, genome-wide association (GWA) studies in HBV did not detect a role for IL28B but a role for human leucocyte antigen-DP variants for HBV persistence (6). Still, this would not rule out a role of interleukin (IL)28B at a significance level below the threshold of GWA studies. A recent North American study addressed specifically the role of rs12979860 SNP within the IL28B region for the spontaneous clearance of HBV. A total of 226 individuals with HBV persistence were compared with 384 with HBV recovery, among whom 75% were Whites and 20% were Blacks. The IL28B SNP was not found to be associated with HBV overall or in analyses stratified by ethnicity, but about one-fifth of the subjects were also chronic HCV carriers and 69% of the subjects were human immunodeficiency virus positive (7). In this issue of the Journal Liver International Li report, an interesting study from China involving 203 individuals with chronic HBV infection, 203 individuals with HBV recovery and 203 healthy controls analysed the potential role of IL28B in the course of hepatitis B virus infection (8). They also found no notable association with persistent HBV infection for any of the three highly correlated SNPs rs12979860, rs12980275 and rs8099917 near IL28B, as with the previous study (7). However, among the chronically infected individuals with available viral load data (93 with a high viral load defined as HBV DNA levels ≥5 log and 90 with a low viral load defined as 0.9), where HBV infection is prevalent, and the moderate effect of the allele shown in the study by Li and colleagues, further studies are warranted to dissect the missing heritability in the host control of viral load among individuals with HBV persistence. Whether the heritability of viral load is linked to IL28B will also need to be explored.
SDGs
Type
editorial