An Increase in Expression of SOCS1 Gene with Increase in Hepatitis C Virus Viral Load

J Interferon Cytokine Res. 2018 Mar;38(3):122-128. doi: 10.1089/jir.2017.0129.

Abstract

Hepatitis C virus (HCV) is a global health problem, with an estimated prevalence of >185 million infections worldwide. About 399,000 people die every year because of HCV-associated liver complications such as liver cancer, liver cirrhosis, and hepatocellular carcinoma. Pakistan has the second-highest prevalence of HCV. The treatment of this life-threatening disease has always been a challenge, but the recent development of direct acting antivirals (DAAs) has offered hope to so many patients with this infection. Although DAAs have dramatically improved virologic clearance, their cost is prohibitive in low economic settings, which is why interferon (IFN) is still used in Pakistan and other developing countries. Many genes-specifically, interferon stimulating genes-alter treatment response. This study recruited 93 participants and used quantitative real-time polymerase chain reaction for the quantification of SOCS1 gene messenger RNA (mRNA) in the peripheral blood mononuclear cells of 5 different groups: IFN treated, IFN resistant, IFN nonresponders treated with DAAs, untreated, and healthy controls. A moderate positive correlation (rs = 0.492) was observed between viral load and SOCS1 mRNA expression level. Our results suggest the over-expression of SOCS1 in PBMCs of IFN non-responders as compared to responders and DAA treated IFN non-responders.

Keywords: DAA; GAPDH; IFN; SOCS1 expression.

MeSH terms

  • Adult
  • Cytokines / pharmacology
  • Female
  • Hepacivirus / drug effects
  • Hepacivirus / genetics
  • Hepacivirus / physiology*
  • Humans
  • Leukocytes, Mononuclear / drug effects
  • Leukocytes, Mononuclear / metabolism
  • Ligands
  • Male
  • Middle Aged
  • Suppressor of Cytokine Signaling 1 Protein / genetics*
  • Suppressor of Cytokine Signaling 1 Protein / metabolism
  • Up-Regulation / drug effects
  • Viral Load* / drug effects

Substances

  • Cytokines
  • Ligands
  • SOCS1 protein, human
  • Suppressor of Cytokine Signaling 1 Protein