Table 3.

Summary of innate and adaptive immune evasion by hepatitis C virus (HCV) infection and hepatitis B virus (HBV) infection.

	Innate immune evasion	Adaptive immune evasion
HCV	RIG-I and TLR3 signaling leading to induction of type I IFNs and proinflammatory cytokines Induction of interferon stimulated genes Exhaustion of type I IFN signalling NS3/4a cleavage of RIG-I and TLR3 adapter proteins HCV core, NS5a and E2 protein interference with JAK-STAT signaling NK cell dysfunction with polarization towards cytotoxicity and impaired IFN-γ production	CD4 T cell depletion early during infection, with weak or absent CD4 T cell responses Chronic antigenic stimulation leading to CD8 T cell failure characterized by weak responses, lack of proliferation, exhaustion and selection for escape mutants Selection for neutralizing antibody escape variants (limited effect)
HBV	Weak innate immune responses NK cell dysfunction with polarization towards cytotoxicity and impaired IFN-γ production	CD4 T cell depletion early during infection, with weak or absent CD4 T cell responses CD8 T cell failure characterized by non-specific responses, exhaustion and deletion Reduced CD4 T helper 2 cells required for B cell expansion Down regulation of co-stimulatory molecules on B cells Functional impairment of B cells

RIG-I = Retinoic acid-inducible gene I

TLR = Toll-like receptor

IFN = Interferon

NK = Natural killer