Ribavirin (Tribavirin) is a synthetic nucleoside analog of ribofuranose with activity against hepatitis C virus and other RNA viruses.

ALT, AST activities and bilirubin levels are significantly loared by administration of JAT in combination with interferon and ribavirin (p<0.01). JAT, interferon or ribavirin alone with CCl4, livers appear to exhibit some liver protection against CCl4 as evident by the presence of normal hepatic cords, absence of necrosis and lesser fatty infiltration. Groups treated with JAT, Peg-interferon and ribavirin separately or in combination shows reduction in the expression of TGF- β and Bax. In the group treated by triple combination of interferon, ribavirin, and JAT, the expression level of p53 is markedly reduced[6]. Ribavirin capsules (400 mg of ribavirin)-treated Wistar rats show a significant decrease in activin-A and significant increase in follistatin at the serum and liver levels. Ribavirin has strong antiviral activity only when ribavirin is combined with either IFN-α or Peg-IFN-α[7]. Ribavirin (40 mg/kg, p.o.) significantly improves the antiviral efficacy of CM-10-18 in mice. Ribavirin inhibits DENV virus infection in cultured cells, but it is ineffective in reducing viremia in monotherapy[8].

The effect of Ribavirin on microglial cell viability is evaluated by the sulforhodamine B (SRB) chemosensitivity assay. Briefly, LPS-stimulated microglial cells are incubated for 48 h in the presence or absence of Ribavirin. Afterward, the cells are fixed in 10% (w/v) trichloroacetic acid for 1 h at 4°C, rinsed in tap water and stained with 0.4% (w/v) SRB in 1% acetic acid (100 μL/well) for 30 min at room temperature (RT). The cells are then rinsed three times in 1% acetic acid to remove the unbound stain. The protein bound stain is extracted with 200 μL 10 mM Tris base (pH 10.5) per well. The optical density is read at 540 nm, with correction at 670 nm. The results are presented as percentage of the control (non-stimulated/untreated microglial cells), that is arbitrarily set to 100%.