For example, COX-2 inhibition in VSV-infected mice increases plasma IFNγ and IL-12 levels [23], and treatment of hepatitis B or C patients with the COX-1/COX-2 inhibitor indomethacin increases serum levels of the IFN response product 2′5′-oligoadenylate synthetase-1 [24]. The gene discussed is OAS1; the disease is hepatitis B virus infection.