Currently IFN is the only drug with anti-HCV effect on chronic hepatitis C treatment, but only 16%-20% of patients achieved sustained response (SVR) with common IFN treatment alone, although the developed pegylated interferon overcame the rapid absorption after subcutaneous injection, fluctuating serum concentration, wide systemic distribution, high renal clearance and short serum half-life of common IFN, making the degree of antiviral insufficiency and other defects, but also can only increase the SVR to 29%-42%, even if the dose of PEG-IFN is increased, it is difficult to significantly improve the response rate. Ribavirin, a guanine analogue synthesized in 1970, has anti-RNA and DNA viral activity, but in antiviral therapy for HCV, it only resulted in a hypo-ALT effect in less than half of the patients, and no clearance of HCV even with prolonged treatment. clinical results from four large randomized controlled trials in 1998 showed that the combination of RBV and IFN, both for primary patients or retreatment of patients who relapsed after IFN treatment significantly improved the efficacy of anti-HCV therapy. Although RBV has no effect on the first and second phases of altered viral kinetics when combined with IFN, it does attenuate the rebound of viral levels between IFN applications, and this effect correlates with blood RBV concentrations and half-life, with 90% SVR achieved when blood concentrations reach 15µM/L is, even in those with high viral loads of genotype 1. In IFN combined with RBV anti-HCV therapy, the possible mechanisms of action of ribavirin are (1) intracellular phosphorylation of the ribavirin product mildly inhibits the HCV NS5B RNA polymutase activity. (2) Acting as a mutagen of the virus, leading to coding errors in the viral genome and reducing the production of infectious virus. (3) Inhibits the activity of host hypoxanthine nucleoside monophosphate dehydrogenase (IMPDH), leading to depletion of the intracellular GTP pool and affecting viral RNA synthesis. (4) More importantly, RBV has immunomodulatory effects, shifting the viral immune response from Th2 to Th1, increasing the production of Th1-type cytokines (IL-2, IFN-g) and TNF-a, inhibiting humoral immune responses such as antibody-mediated cytotoxicity, thereby increasing the host T cell-mediated immune response and increasing the clearance of virus-infected cells, which is the main mechanism by which RBV improves anti This is the main mechanism by which RBV improves SVR in anti-HCV therapy. IFN combined with RBV treatment reduces the risk of no sustained response in IFN primary, relapsed and non-responders retreated for chronic hepatitis C by 26%, 33% and 11%, respectively. It also contributes to histological improvement. Although the SVR of regular IFN for chronic hepatitis C was only 16C20%, the combination of RBV increased the efficacy to 35C40%. RBV only mildly increased the viral response rate at the end of treatment, but increased the SVR by a factor of 1. In one study, the viral response rates at the end of anti-HCV treatment were 59%, 52% and 69% for PEG-IFN alone, regular IFN + RBV and PEG-IFN + RBV, respectively, with the highest sustained response rate (56%) for PEG-IFN a-2a + RBV and higher for regular IFN + RBV (44%) for overall patients. PEG-IFN monotherapy (29%). SVR was also significantly higher with regular IFN + RBV (33%) than with PEG-IFN monotherapy (13%) in those with high genotype 1 viral load. The results suggest that RBV mainly increases the rate of sustained response and decreases relapse at the end of treatment. Therefore, the role of RBV cannot be doubted by the viral response rate at the end of treatment or not. For the treatment of general IFN, especially PEG-IFN, both economical and efficacy considerations should focus on the combination of RBV, while for the antiviral treatment of general IFN in patients with chronic hepatitis C, the combination of RBV should be even more important. The kinetic changes of RBV on the virus during treatment are genotype-dependent, and the synergistic antiviral effect of IFN and RBV is mainly seen in genotype 1 patients. In genotype 1 patients, treatment with high doses of RBV resulted in maximum SVR, and the applied dose of RBV was positively correlated with SVR under the conditions of standard PEG-IFN dosage and 48 w course of treatment, while no such correlation was found for genotypes 2 and 3, and standard and low doses of RBV did not affect SVR. Therefore, for antiviral treatment of genotype 1 HCV, the dosage of RBV should be The anti-HCV treatment with PEG-IFN+RBV has a dosage of 1200 mg/d for genotype 1, weight 75 kg, while the European recommendation is 1200 mg/d for weight 85 kg. The US recommendation is a fixed dosage of 800 mg/d for RBV in combination with PEG-IFN, which is due to the side effects of RBV. side effect considerations. The HCV genotype in Chinese patients with chronic hepatitis C is about 80% genotype 1, but there is no recommendation for the dosage of RBV in Chinese patients with chronic hepatitis C. The application of RBV has some side effects and some patients have difficulty completing the entire course of treatment. The main side effect of ribavirin is the lack of enzymes for dephosphorylation of erythrocytes, which causes accumulation of RBV phosphates in erythrocytes, inhibits ATP-dependent substance utilization, affects oxidative cellular respiration, and shortens the half-life of erythrocytes through extravascular blood fusion, resulting in reversible hemolytic anemia. The occurrence of such side effects is highly individualized and should be closely monitored, requiring RBV dosage selection and dose adjustment according to HCV genotype and kinetic changes in viral load during treatment. Some studies have shown that even in patients who obtained virological response in 24W of PEG-IFN+RBV treatment, stopping RBV treatment will significantly increase the rebound of virus during treatment and the recurrence rate of virus after the end of treatment, therefore, it is important not to stop RBV treatment categorically due to the occurrence of side effects, and patients should be treated according to the degree of side effects without affecting the efficacy of The patient should be treated appropriately according to the degree of side effects, otherwise the antiviral efficacy will be significantly reduced. For those who need to adjust the dose of RBV due to the occurrence of side effects, it is best to reduce the dose after the patient has achieved virological response, and reducing the RBV dose after 20 weeks will not affect the occurrence of SVR, but should be done throughout the treatment. Since the combination of RBV can significantly improve the efficacy of anti-HCV therapy with common IFN or PEG-IFN, the combination of RBV and IFN should be emphasized regardless of the economics and efficacy considerations, but the RBV dose should be selected according to HCV genotype and patient weight, while the management of its side effects occurrence can be adjusted according to the viral response during treatment to complete the whole course of treatment with a view to obtaining the maximum chance of SVR.