In compensated cirrhosis, SVR, biochemical response and histological response were achieved with either plain IFN or PEG-IFNα combined with RBV treatment. One study showed that 8%, 15%, and 30% of the regular IFN group, 90 μg PEG-IFN group, and 180 μg PEG-IFN group achieved SVR at 72 weeks, respectively [14], and although SVR was relatively low in patients with cirrhosis compared with non-cirrhotic patients, it still delayed the progression of cirrhosis in these responders and relatively reduced the incidence of hepatocellular carcinoma. It is important to note that patients with compensated cirrhosis should be closely monitored for adverse events during treatment. There is no consensus that liver transplantation should be considered first for patients with decompensated cirrhosis and whether antiviral therapy should be given. The Asia-Pacific Hepatitis C Expert Consensus published in 2007 and the American College of Hepatology Hepatitis C Guidelines published in 2009 both concluded that liver transplantation should be considered for the treatment of decompensated hepatitis C cirrhosis and that antiviral therapy should be tried only in experienced liver disease centers. Because most patients have pre-treatment granulocytopenia, thrombocytopenia and anemia, antiviral therapy can exacerbate these symptoms. Therefore, there is a high risk of treatment. However, it should be noted that recent data have shown the feasibility of antiviral therapy in decompensated cirrhosis. Iacobellis et al. gave PEG-IFN α-2b (1.0 μg/kg per week) in combination with standard doses of RBV for 24 weeks in patients with decompensated cirrhosis (all genotypes included) and achieved an overall SVR of 19.7%, including 43.5% in genotypes 2 and 3 infected patients Therefore, antiviral therapy for patients with decompensated hepatitis C cirrhosis deserves to be explored, especially with regard to enrolled patients, treatment duration, drug dose, and related side effects, and more clinical trials are needed to further investigate the best benefit and least harm. However, the ultimate goal is not only to achieve SVR, but also to create conditions for liver transplantation or to improve the prognosis for patients who cannot be transplanted. Antiviral therapy in patients with fatty liver, metabolic syndrome, and insulin resistance Hepatic steatosis is an independent risk factor for failure of antiviral therapy in patients with chronic hepatitis C, independent of viral genotype; obesity is also a factor affecting low response to antiviral therapy in chronic hepatitis C. Obese patients with chronic hepatitis C with a body mass index over 30 kg/m2 are four times less likely to achieve SVR than non-obese patients . In a multicenter, randomized, double-blind, placebo-controlled study reported at the 2008 American Liver Congress, 123 patients with genotype 1 viral infection with insulin resistance on primary IFN were randomized to two groups receiving either PEG-IFN α-2a in combination with RBV based on metformin [425 mg three times daily, switching to 850 mg three times daily until the end of treatment after 4 weeks ( 48 weeks)], or PEG-IFN α-2a combined with RBV conventional treatment, SVR was not significantly different between the two groups by ITT analysis and PP analysis, but the reduction in insulin resistance index (HOMA-IR) assessed by the homeostasis model was significantly different between the two groups, by 1.8 and 0.6, respectively. but in the subgroup analysis, it was found that the difference in SVR after the addition of metformin in female patients were significant, 57.7% and 28.6%, respectively. The prevalence of fatty liver and metabolic syndrome in China is significantly higher than before. The relationship between fatty liver and HCV infection and the prevalence of fatty liver in patients with chronic hepatitis C is not well understood by us, which requires further studies to clarify and observe its impact on antiviral therapy and establish an effective antiviral treatment regimen. Diagnosis and treatment of hepatitis C virus infection in children HCV-infected mothers can passively transmit their own anti-HCV to the fetus via the placenta and umbilical cord during delivery; therefore, newborns of HCV-positive mothers cannot be diagnosed with anti-HCV positivity as hepatitis C infection; if HCV infection is diagnosed by anti-HCV it should be tested after 18 months of age or at 1 to 2 months of age by HCV RNA test to make the diagnosis. Based on the available evidence-based medical evidence, pediatric patients older than 2 years of age should be treated with IFN alpha-2b at 60 μg/m2 per week for 48 weeks in combination with RBV 15 mg/(kg?d). Diagnosis and treatment of patients with co-infected HIV Because HIV and HCV infections share a common transmission route, all HIV-infected patients should be tested for anti-HCV, especially those with a history of syringe sharing, and some HIV-infected patients are often negative for anti-HCV due to immunocompromise and should be tested for HCV RNA to aid in diagnosis, especially for HIV infection with coexisting unexplained liver disease. Treatment of patients with mixed HIV and HCV infection should begin with clarification of which is more severe, HIV or HCV infection, and if the severity of liver disease and the likelihood of a treatment response outweigh the consequences of adverse events, then hepatitis C should be treated, and the initial regimen should be PEG-IFNα in combination with RBV for 48 weeks, but for patients receiving zidovudine or dehydroxymethyldeoxyinosine treatment, one should switch to other nucleoside analogues to avoid aggravating liver damage. Treatment of organ transplant patients Those with histologic evidence after liver transplantation may be considered for antiviral therapy with or without PEG-IFNα in combination with RBV, but should be closely monitored. Antiviral therapy for liver transplantation in chronic hepatitis C end-stage liver disease is divided into four conditions: pre-transplantation therapy, prophylaxis, early post-transplantation therapy, and delayed post-transplantation therapy [9]. Pre-transplantation therapy is used for patients with mild decompensation or mainly primary patients with low model of end-stage liver disease (MELD) scores, and is treated with a gradual increase in IFNα to bring HCV RNA below detectable levels before transplantation; prophylaxis uses monoclonal antibodies to hepatitis C globulin and hepatitis C virus envelope region 2, but no significant effect has been obtained; early post-transplantation therapy is further divided into 8 weeks post-transplantation and The latter is used for those with predicted progressive disease, while the former is used for those with high-risk progressive disease; delayed post-transplant treatment is routinely recommended for patients with progressive disease, or severe histological or biochemical alterations to reduce the risk of disease progression [19]. Antiviral therapy should not be given to heart, lung, or kidney transplant patients, as IFNα will promote graft rejection and lead to graft inactivation. IFNα therapy may be considered only in the event of fibrous sideroblastic hepatitis, when the benefits of antiviral therapy outweigh the adverse consequences.