Table 1.

Differential effects of type I and III IFNs on enteric viruses.

Virus	Type I IFN	Type III IFN	References
Norovirus (NoV)	Prevents lethality from acute MNoV infection Controls systemic spread of persistent MNoV	Controls persistent intestinal infection by restricting IEC tropism Therapeutic administration clears persistent MNoV and prevents transmission of acute strain Associated with interactions between microbiota and NoV	[45,52,54,56,58,61,62,63]
Reovirus	Robustly induced by infection in vitro Prevents lethal infection in vivo	Preferentially induced in some cell types Controls intestinal levels and shedding into stool	[45,48,64,65]
Rotavirus (RV)	Treatment decreases local spread and replication in intestinal enteroids Controls diarrhea and systemic replication in vivo Combined deficiency of IFN-α and IFN-γ signaling increases mortality in suckling mice Postnatal mice are responsive to IFN-β treatment, but this diminishes with age	Robustly induced in human enteroids Controls infection in the intestine, acting synergistically with IL-22, and can effectively treat infection in mature mice	[27,47,66,67,68,69]
Adenovirus (AdV)	Induced by in vitro infection Antiviral when administered in vitro	Unknown	[70,71,72]
Murine cytomegalovirus (MCMV)	Induced by infection IFN-β has most effective antiviral effect of type I IFNs	Induced by infection Robust antiviral effects against MCMV	[73,74]