Table 1:
Immune compartment and status in chronic HCV | IFN-based therapy | Restoration after successful treatment DAA therapy |
---|---|---|
Viral sensing (PRR-mediated signalling) | ||
Impaired signalling Altered early IFN response |
Not restored (23) | Restored signalling and response to IFN (21,23) |
NK cells | ||
Low cytokine production ↑ activation ↑ degranulation ↓ response to IFNα |
↑ NK function predictive of SVR (24) | Restoration of NK phenotype (25,26) |
DC | ||
↓ Frequency ↓ Pro-inflammatory cytokines ↑ Immunosuppressive cytokines |
Impaired DC associated with treatment failure (27) Restored allogenic responses (28) |
Restored PRR-mediated defect (29) |
Monocytes and macrophages | ||
↓ IL-18 production Impaired differentiation of monocytes into M1 and M2 macrophages |
Not tested | Partial restoration of macrophage polarization (30) |
MAIT cells | ||
↓ Frequency in liver Global activation of cells ↓ Response to bacteria |
↑ MAIT activation (31) ↑ Frequency (31) |
Partial normalization of frequency (32) Reduced liver inflammation (32) No restoration of response to bacteria (32) |
Note: ↑= increased; ↓= decreased. DAA = Direct-acting antiviral; DC = Dendritic cell; HCV = Hepatitis C virus; IFN = Interferon; IL = Interleukin; MAIT = Mucosal-associated invariant T cell; NK = Natural killer; PRR = Pattern recognition receptor; SVR = Sustained virologic response