, Volume 33, Issue 6, pp 1110-1116
Date: 24 May 2013

SOCS-1 Promoter Methylation and Treatment Response in Chronic Hepatitis C Patients Receiving Pegylated-Interferon/Ribavirin

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Suppressor of cytokine signaling-1 (SOCS-1) is a negative regulator of the Janus kinase/signal transducer and activation of transcription pathway. The purpose of this study was to investigate the relationship between methylation of SOCS-1 and sustained virologic response (SVR) in chronic hepatitis C (CHC) patients treated with pegylated interferon (PEG-IFN)-alpha and ribavirin (RBV).


In total, 106 CHC patients treated with PEG-IFN-alpha and RBV were included. Serum samples were obtained at baseline (P), end of treatment (EOT), and 6 months post treatment (F6). Methylation status of the promoter region of SOCS-1 was examined by quantitative methylation specific PCR (qMSP).


Median baseline methylation level of SOCS-1 was −0.95 log10 copies/mL, which increased to 0.57 log10 copies/mL at EOT and then returned to −0.57 log10 copies/mL at F6 (baseline vs EOT, P < 0.001; EOT vs F6, P < 0.001). The overall SVR was 75.5 %. Univariate analysis indicated that SVR was significantly associated with genotype, baseline HCV RNA, body mass index (BMI) and higher EOT SOCS-1 methylation. Multivariate analysis confirmed that the SVR was significantly associated with genotype (OR: 13.40, 95 % CI: 1.73–103.58, P = 0.013), baseline HCV RNA (OR: 0.19, 95 % CI: 0.06–0.59, P = 0.004), BMI (OR: 0.73, 95 % CI: 0.56–0.96, P = 0.022), and EOT SOCS-1 methylation (OR: 1.71, 95 % CI: 1.11–2.62, P = 0.014).


CHC patients with significantly higher SOCS-1 methylation at the end of treatment had better SVRs. The role of SOCS-1 methylation in affecting treatment response deserves further investigation.