Abstract:
Hepatitis C Virus (HCV) is a viral infectious disease that affects an estimated
130-170 million people worldwide. Most of those infected (80%) go on to develop a
chronic infection. Until recently, the standard treatment for those with chronic HCV was
a combination of pegylated interferon-α (PEG-IFN-α) and the antiviral ribavirin (RBV).
In treatment-naive genotype 1 HCV patients, the combination of PEG-IFN-α and RBV
typically leads to Sustained Virological Response (SVR) rates between 47% and 54%. In
a number of recent studies, the IL28B gene has been shown to play an important role in
the outcome of HCV treatment. A particular single nucleotide polymorphism (SNP) on
chromosome 19q13 (rs12979860), commonly referred to as the “IL28B variant,” is
strongly associated with SVR or lack of it. Metabolic syndrome (MetS) is a group of
medical disorders usually associated with obesity. Some evidence suggests that HCV
infection exacerbates this condition, possibly by causing increased insulin resistance (IR) and promoting visceral obesity even further. Metabolic abnormalities have also been
shown to influence patients’ response to HCV treatment. Recent, but not conclusive,
evidence suggests that, in addition to influencing response to HCV treatment and SVR
rates, the IL28B genotypes may be associated with metabolic confounders of HCV such
as insulin resistance and metabolic syndrome. This study investigates a possible
connection between IL28B genotype and MetS components in patients with and without
chronic HCV. As expected, correlations between IL28B genotype and SVR, as well as
between metabolic profile and SVR, were revealed. Further studies of a connection
between IL28B genotype and metabolic outcomes are warranted.
