Table 1.

Roles of hepatitis C virus (HCV) proteins on the evasion of the intracellular antiviral response.

Viral Factor	Function	Reference
N3-4A	cleaves MAVS, to impair production of IFNs and proinflammatory cytokines	[31,37,52,53,54,55,57]
	cleaves TRIF, to impair production of IFNs and proinflammatory cytokines	[28,58]
	inactivates Riplet, inhibiting RIG-I and IRF3 activation	[62,63]
	binds to LUBAC, impairing the polyubiquitynation of NEMO required for NF-κB activation	[66]
	induces degradation of STAT1, impairing the expression of antiviral effectors	[67]
	binds to TBK1, impairing IRF3 activation	[59,60,61]
Core	blocks NF-κB, to suppress inflammatory response	[98,99]
	targets JAK/STAT pathway by targeting STAT1 and STAT2, inhibiting the production of ISGs	[52,67,104,105,106,107,108,110,111,112]
E2	interacts with PKR, repressing its antiviral effects	[89]
NS5A	interacts with PKR, repressing its antiviral effects	[88,90]
	induces NAP1L1 degradation, inhibiting gene transcription essential for RIG-I- and TLR3-mediated responses	[91]
	impedes RIG-I- and MDA5 activation, impairing IFNs expression	[33]
NS4B	downregulates TRIF protein, inhibiting TLR3 signaling	[68]
	interacts with STING, inhibiting the production of IFNs	[69,70]
p7	interacts with IFI16-16, inhibiting its antiviral function	[114]