The antiviral treatment of chronic hepatitis C has been going on for more than 10 years, especially in the last 10 years of clinical trials and practical studies, which established sustained viral response (HCV RNA in the blood remains below the detection line 24 weeks after stopping treatment) (SVR) as the goal of antiviral treatment for chronic hepatitis C. The use of ribavirin and pegylated interferon has established ribavirin and pegylated interferon in the antiviral treatment of chronic hepatitis C because of their significant improvement in antiviral efficacy. Many factors can influence the efficacy of antiviral therapy for chronic hepatitis C. Viral changes in antiviral therapy are significantly predictive and correlated with the achievement of SVR. The principles of response-guided therapy (RGT) should be properly understood and applied. Standardization and standardization of therapy: Among the factors affecting the antiviral therapy for chronic hepatitis C, there are unchangeable factors such as the patient’s age, gender, degree of liver disease, IL-28B genotype, viral load and genotype, and adjustable factors such as the type of interferon preparation and its dose, ribavirin dose and usage, and the duration of therapy. (1) Standardization of drugs and doses: Because pegylated interferon combined with ribavirin allows patients to achieve higher SVR than regular interferon combined with ribavirin, or pegylated interferon monotherapy, in 2002, various medical groups recommended pegylated interferon combined with ribavirin for chronic hepatitis C. Thus, pegylated interferon combined with ribavirin became the The standard of care for chronic hepatitis C is pegylated interferon in combination with ribavirin. Although patients in China are often treated with plain interferon in combination with ribavirin for economic reasons, standard therapy should be used whenever available in order to obtain a higher probability of SVR. The results of health economics studies have shown that standard therapy is more valuable than treatment with plain interferon combined with ribavirin. Because both pegylated interferon dose and ribavirin dose can significantly affect outcome, standardized therapy should also include standardization of pegylated interferon dose and ribavirin dose. PEGylated interferon alpha 2a 180 μg, or pegylated interferon alpha 2b 1.5 mg/kg, should be administered subcutaneously once a week, unless dose adjustments are made for those who cannot tolerate the side effects, but the standard dose should be maintained as much as possible if it can be maintained. It is also important to note that weekly injections should not be used to extend the interval between injections at will. The standard dose of ribavirin should be determined by the patient’s HCV genotype and body weight, with a standard daily dose of 800 mg for patients with HCV genotype 2/3. For non-genotype 2/3 patients, the standard dose of RBV is 10.5 mg/kg/day, although earlier studies recommended 10.5 mg/kg/day, and 15 mg/kg/day for genotypes 1, 4 and 6. 2) Patient education: Another important factor affecting the efficacy of anti-HCV therapy is patient compliance, and patients with good compliance are better able to cooperate with their physicians. Patients with good compliance are better able to cooperate with their physicians and ensure the dose and duration of drug therapy to increase the probability of SRV acquisition. Therefore, patient education is required prior to initiating treatment. Good patient education includes informing patients of the purpose of treatment, the content and timing of regular monitoring during treatment, the regimen that must be adhered to in order to achieve maximum SRV, and the importance of ensuring that the medication dose is standardized for SRV. More importantly, patients should be informed that this is a disease that can be cured through treatment and the possible long-term benefits of treatment in order to increase their confidence in treatment. Proper understanding and application of RGT principles: Although the effect of antiviral therapy for chronic hepatitis C is influenced by multiple factors, the ultimate effect is expressed in the change of HCV RNA. Among the factors affecting SVR, the most important ones are HCV genotype (genotype 1 treated for 48 weeks and genotype 2/3 treated for 24 weeks) and viral load, host IL=28B genotype, and when the RVR obtained after one month of PEG-IFN α/RBV/ boceprevir treatment is also taken into account for analysis, the acquisition of RVR can eliminate other baseline factors ( age, sex, IL-28B, genotype and viral load, etc.) as predictors of SVR, and guiding treatment (RGT) and optimizing treatment regimens according to viral response during treatment are fundamental to ensure maximum SVR acquisition. (1) Following the principles of RGT is essential to ensure SVR acquisition: Based on the detection of baseline HCV RNA levels, changes in HCV RNA levels during treatment must be monitored and further treatment guided according to the on-treatment viral response. The prediction of SVR by on-treatment viral response allows early identification of patients who cannot obtain SVR to avoid unnecessary treatment; timely adjustment of treatment regimen for those with poor response to obtain SVR; and enables patients with good response to avoid unnecessary prolonged treatment on the basis of maximizing SVR rate. The viral response during treatment can be divided into Sustained virological response (SVR); Rapid virological response (RVR); Early virological response (EVR); Delayed virological response (DELAYED); and the viral response (EVR). Delayed virological response (DVR); Partial nonresponse (PR) and Breakthrough (BT); Null response (NR). ? We set out clear requirements: 1) for patients with no response, partial response and viral breakthrough during treatment, treatment should be stopped due to difficulties in obtaining SVR under the current regimen; 2) the lower limit of HCV RNA detection reagents must be ≤50 IU/ml; 3) regimens that can obtain SVR must bring HCV RNA below the detection line and maintain it until the end of treatment; 4) HCV RNA negative duration determines the probability of SVR acquisition. (2) Possible errors in SVR prediction caused by domestic HCV RNA detection reagents in clinical practice: Since viral load reaching the lower limit of detection is a prerequisite for obtaining SVR, and the current RGT principle is based on HCV RNA content detection reagents with sensitivity reaching the lower limit of detection ≤50 IU/ml, therefore, reagents with poor sensitivity often bring errors in the judgment of the required course of treatment and SVR prediction brings some error. Some patients whose HCV RNA content has not reached the lower limit of detection by sensitive reagents during treatment are often incorrectly judged as RVR or cEVR (complete early viral response, i.e. the virus reaches below the detection line at 12 weeks of treatment) due to the insensitivity of domestic reagents, and the course of treatment is judged according to standard reagents, which often leads to relapse due to insufficient course of treatment. The results of the “11th Five-Year Plan” major project showed that 37.33% and 20.83% of patients with non-RVR and non-cEVR detected by Roche COBAS TaqMan? HCV Test were detected by domestic reagents as RVR and cEVR, respectively, and genotype 1 patients among these patients, such as stopping the drug after 48 weeks of treatment according to the guidelines would have led to relapse in many patients, as it has been noted that to maximize the probability of obtaining SVR, the virus must reach <50 IU/ml and maintain treatment for more than 44 weeks. In order to avoid treatment failure due to HCV RNA detection reagent errors during antiviral therapy in Chinese patients with chronic hepatitis C, it is advisable to use international standard detection reagents (lower limit of detection ≤50 IU/ml) at key monitoring time points (4, 12 and 24 weeks of treatment). 3) Shortening the course of antiviral therapy monitored by Chinese-made HCV RNA detection reagents is not recommended: Because of the many side effects of PEG-IFN α/RBV therapy, some patients have difficulty tolerating it and thus often wish to shorten the course of therapy, although some studies have shown that in patients with low viral load baseline (< 400 000 IU/ml) and RVR acquisition, it is possible to shorten the course of therapy in patients with genotype 2/3 Even when RVR is obtained, SVR is still better with the standard regimen than with the shortened regimen, and some studies have even shown that the regimen should be extended to 48 weeks in genotype 2/3 patients who do not obtain RVR. For genotype 1 patients, while some studies have shown that SVR for 24 weeks of treatment is similar to 48 weeks of treatment for those with low viral load baseline (< 400 000 IU/ml) and who have achieved RVR, studies from Taiwan have shown that 48 weeks of treatment is required for genotype 1 patients in China with or without RVR. The above prerequisites for shortening the treatment course are low viral load and obtaining RVR. Since most of the Chinese-made reagents do not meet the sensitivity of international standard reagents (lower limit of detection ≤50 IU/ml) and even patients who obtain RVR need to be treated for 48 weeks, and Chinese-made reagents tend to detect high viral load as low viral load and often detect non-RVR as RVR results, it is not recommended to The shortened course of treatment for patients monitored with domestic reagents is therefore not recommended. Not only is a shorter course of treatment not recommended, but a standard course of treatment is also recommended even when monitored by more sensitive detection reagents to increase the probability of obtaining SVR. The guidelines for antiviral therapy for chronic hepatitis C from Germany/Austria/Switzerland define RVR, cEVR and DVR as HCV RNA <12-15 IU/ml and still recommend a standard course of therapy under this test to maximize the probability of SVR acquisition. (4) The need to extend the course of treatment in patients with poor response: SVR acquisition is determined by reaching the lower limit of detection for HCV RNA during treatment, the duration of maintenance treatment at the lower limit of detection, and whether relapse occurs after stopping treatment. After reaching the lower limit of detection, a longer duration of maintenance therapy helps to reduce the relapse rate and thus improve SVR rates, and in slow responders, where the virus is relatively insensitive to treatment response, it is even more important to extend therapy to ensure that more patients can reach the lower limit of detection, while ensuring that there is sufficient duration of maintenance therapy below the line of detection to reduce relapse rates and improve SVR. with the use of standard detection reagents, three Three European studies and one meta-analysis study showed that extending the treatment course to 72 weeks for genotype 1 slow responders significantly reduced relapse rates and improved SVR rates. Patients with genotype 2/3 who do not achieve RVR should be treated for up to 48 weeks. Since the sensitivity of our domestic HCV RNA quantification reagents is often less than that of international standard reagents, under the RGT guidelines, the course of treatment should be extended for patients with EVR, especially DVR, to maximize the probability of obtaining SVR. In conclusion, in order to maximize SVR acquisition, antiviral therapy for chronic hepatitis C should be standardized using PEG-IFN/RBV, which includes standardization of drug doses, and the RGT principle is based on HCV RNA detection reagents with a lower limit of detection ≤50 IU/ml. In clinical practice, standardized treatment should be carried out according to the RGT principle. Since it is still difficult for our domestic HCV RNA testing reagents to reach the lower limit of detection of ≤50 IU/ml, it is not recommended to shorten the treatment course for patients when using domestic reagents for testing, and the course of treatment should be extended to 72 weeks for patients who have poor response and reach the lower limit of detection only at 12 or 24 weeks in order to improve the SVR acquisition rate.