Table 1.
Hepatitis viruses have developed multiple strategies to disrupt the immune response by hijacking the SOCS system
| Virus | SOCS protein | In vivo or In vitro | Viral proteins | Mechanism | References |
|---|---|---|---|---|---|
| HCV | SOCS1/3 | Hep-G2 cell | HCV core protein | Inhibit IFN-α induced expression of 2′,5′-OAS and MxA | [40] |
| SOCS3 | patients | HCV genotype 1 | Reduce the biological response to IFN-α | [43] | |
| SOCS1 | PBMC | HCV core protein | Dysregulate T- and B-cell signalling | [44–47] | |
| SOCS | Myeloid DCs | HCV genotype 3 | Diminish capacity to present antigen | [49] | |
| SOCS3/7 | Huh-7 | HCV genotype 3 | Downregulation of IRS1 and IRS2 | [52–54] | |
| HBV | SOCS3 | Huh-7 and liver specimens from HBV-infected patients | adenoviral AdHBV (genotype A) | Dysregulate STAT/SOCS-signalling | [58] |
| SOCS1 | HepG2.2.15 cells and PBMC | HBV antigen, HBeAg | Promote inflammatory cytokine production | [60] | |
| SOCS1 | plasmacytoid dendritic cells | HBsAg | Inhibition of the IFN-α production | [61] | |
| SOCS1/3 | HBV transgenic mice | CTP-HBcAg18-27-tapasin | enhance T cell immune responses | [62–64] |
Viral proteins disrupt the host’s immune response by hijacking different SOCS proteins in vivo or in vitro.