Interferon has been discovered for 50 years, and with the development of clinical medical research, it is now widely used in antitumor and antiviral therapy. In antiviral therapy, especially interferon antiviral therapy for chronic hepatitis B and chronic hepatitis C, great progress has been made in recent years. Interferon is a naturally occurring biomolecule in the human body, which has a dual effect of immunomodulatory and direct antiviral activity, and has different antiviral effects on different viruses due to their different biological properties. The biological effect of interferon is firstly, it binds to the receptors on the cell surface and exerts its antiviral and immunomodulatory effects through a series of signaling molecules. In the antiviral effect, interferon binds to the receptor and induces the expression of protein kinase, 2′,5′ oligodeoxynucleotide synthase and MxA, which have the ability to explain viral nucleic acid and inhibit viral replication, thus inhibiting intracellular viral replication. The interferons with strong antiviral activity include interferon a. The cell surface interferon a receptors are a1 and a2. interferon a1 has a low binding capacity to the receptor, and its binding capacity can only be increased by accompanying with a2 at any time, so the clinical antiviral effect of interferon a1 is often inferior to that of interferon a2. Since the inhibition of viral replication by interferon-induced antiviral proteins occurs mostly in the cytoplasm, and the inhibition of The antiviral effect of interferon on hepatitis C virus is higher than that on hepatitis B virus because the inhibition of viral replication by interferon-induced antiviral proteins occurs mostly in the cytoplasm, while it is difficult to exert a direct antiviral effect on viruses with an intranuclear replication mechanism. In the antiviral therapy, especially the interferon antiviral therapy for chronic hepatitis B and chronic hepatitis C, has made great progress in recent years. 1, interferon of chronic hepatitis B antiviral therapy. The antiviral treatment of chronic hepatitis B, there are a variety of drug options. Although nucleoside (acid) analogues are easy to use and can better inhibit HBV replication for a certain period of time, thus inhibiting the progression of chronic hepatitis B. However, due to its low HbeAg seroconversion rate, short-term treatment often leads to the recurrence of viral replication after discontinuation of the drug, prolonged application can produce viral drug-resistant mutations and other defects, therefore, interferon is still the choice of antiviral therapy for chronic hepatitis B has certain advantages In particular, PEG-IFN is listed as a first-line drug in the antiviral treatment of chronic hepatitis B in Europe and the United States because it requires only one injection once a week and has higher efficacy than standard interferon. Since the anti-disease treatment of chronic hepatitis B, whether nucleoside analogs or interferons, relies on the host-specific immune response to HBV, patient selection becomes very important, and interferon therapy should be chosen especially for those with low viral load, young age, high serum ALT levels or significant inflammation of liver tissue. Since there are two types of chronic hepatitis B, HbeAg-positive and HbeAg-negative, and there are some differences in their response to interferon antiviral therapy, patients should be treated differently according to their HbeAg status. For HbeAg patients, although the duration of therapy in most clinical trials is 6-12 months, and therefore often leads to the belief that the duration of interferon therapy is 6-12 months, this is in fact incomplete. The treatment of HbeAg-positive chronic hepatitis B should be aimed at achieving certain goals and treatment endpoints. In the case of effective treatment, the primary goal is the reduction of HBV DNA and reaching below the detection line, the further goal is to obtain the disappearance of HbeAg and positive anti-Hbe, and the highest goal is to obtain the disappearance of HbsAg. With the acquisition of these three goals, patients can achieve more significant and long-term results, or even achieve clinical cure. Therefore, clinical treatment should gradually seek the most advanced goal, when the patient only HBV DNA decline or “negative” and end treatment, often lead to relapse, so effective treatment for at least the disappearance of HbeAg and serological conversion, because once the HbeAg serological conversion, more than 80%-90% of patients’ efficacy Bortolotti observed 85 patients with chronic HBV infection and HbeAg seroconversion for 30 years and found that after HbeAg seroconversion for 6 months, 84 patients were cured. After 30 years, 13 cases showed disappearance of HbsAg, 68 cases were considered inactive, and only 4 cases developed HbeAg-negative chronic hepatitis B. No one developed cirrhosis, hepatocellular carcinoma, or death. Yang HI et al. observed 11,893 male patients in Taiwan for up to 9 years, and HbeAg /HbsAg-positive patients had a very significantly higher cumulative incidence of hepatocellular carcinoma than HbeAg-negative and HbsAg-negative individuals (RR=60, 2). In antiviral therapy for HbeAg-positive chronic hepatitis B, only the clearance of HbeAg and HbsAg reflects the clear extent of viral infection of hepatocytes, and when treatment does not achieve HbeAg disappearance and serologic conversion, it often leads to viral relapse, as is the case with nucleoside analogue therapy and also with interferon therapy; therefore, interferon therapy, in order to achieve long-term efficacy, should at least obtain HbeAg seroconversion, and HbsAg disappearance or seroconversion must also result in HbeAg seroconversion. The treatment of HbeAg-positive chronic hepatitis B should be considered to end or not based on whether or not the treatment objective is achieved, with gradual changes in HBV DNA, HbeAg and HbsAg levels or titers during the course of treatment. Serological conversion of HbeAg and HbsAg is achieved. Although interferon therapy does not result in HbeAg seroconversion in every patient, the chance of achieving HbeAg seroconversion increases with longer treatment duration, and although some individual studies have shown that combining nucleic acid analogs or taking sequential therapy with nucleoside analogs may improve the efficacy, large and rigorous clinical trials have yet to be conducted to confirm this. In contrast, interferon therapy for HbeAg-negative chronic hepatitis B differs from that for HbeAg-positive patients in that there is no serologic conversion of HbeAg as an indicator for treatment of HbeAg-negative chronic hepatitis B. Only HBV DNA can be used as the primary evaluation indicator for efficacy. HbeAg-negative hepatitis is characterized by an overall population in which the liver tissue is at a later stage than that of HbeAg-positive, i.e. Interferon therapy is more likely than HbeAg-positive hepatitis to obtain HBV DNA conversion, but the relapse rate is high, only 27% of patients maintain biochemical response after 6-12 months of ordinary interferon therapy, less than 25% of patients get a durable response, to achieve a more durable response should extend the course of treatment to 2 years, Pyroxin treatment for 1 year, 80% of those who achieve HBV DNA response can be maintained for 3 years The duration of treatment should be extended to 2 years. For HbeAg-negative chronic hepatitis B antiviral therapy, although more prone to relapse than HbeAg-positive chronic hepatitis B hepatitis, there are still some patients who can obtain the disappearance of HbsAg and serologic conversion after a period of treatment, whether or how long the course of treatment can obtain the disappearance of HbsAg and serologic conversion should also be determined according to the changes in HbsAg levels during the course of treatment, for In the course of treatment, the HbsAg content should be gradually decreased to extend the course of treatment in order to achieve the disappearance of HbsAg and serological conversion to achieve the highest goal of chronic hepatitis B treatment. 2, the application of interferon in the treatment of chronic hepatitis C. The goal of chronic hepatitis C treatment is to obtain a sustained viral response. Interferon in chronic hepatitis C antiviral therapy is different from anti-chronic hepatitis B virus, because HCV replicates in the cytoplasm, interferon-induced intracellular antiviral protein mechanism of viral replication is stronger than that of hepatitis B virus, but the clearance of the virus still depends on the inhibition of cellular viral replication and the clearance of virus-infected cells by specific immunity. Only intracellular antiviral effect and insufficient cellular immune function is similar to nucleoside analogues for chronic hepatitis B. Relapse after drug discontinuation, while only cellular immune response without inhibition of intracellular viral replication, replicating virus can re-infect other cells, making it difficult to clear virally infected cells. Therefore, in the antiviral treatment of chronic hepatitis C, interferon must be combined in the absence of contraindications Ribavirin, because ribavirin enhances cellular immunity and improves sustained viral response in therapy by reducing relapse rates (the most important goal of chronic hepatitis C treatment). In the treatment of chronic hepatitis C with antiviral therapy, PEG-IFN combined with ribavirin is the current standard of care, and although there are many factors that influence efficacy, the most important ones are the viral genotype in terms of virus, the type and dose of the drug, and the combination and regimen in terms of treatment. Different versions of the guidelines state that patients with genotype 1 should be treated with combination therapy for 48 weeks, while genotype 2/3 should be treated for 24 weeks. However, it is more important to personalize the treatment according to the patient’s viral response in therapy. The first is the individualization of the drug dose, which is 1.5 mg/kg weekly for pegintron and 180 mg weekly for piroxin, especially in high weight patients. Adequate doses should be administered early in treatment. Most studies have shown that interferon and ribavirin doses in the first 12 weeks of treatment can significantly affect efficacy. Significant reductions in drug dose after 12 weeks of treatment also affect efficacy, and therefore, adequate or effective doses should be maintained as much as possible. In addition to dose, timely monitoring of viral response during treatment is the most critical indicator to guide the next step of treatment. One study showed that in PEG-IFN combined with ribavirin, 90% of those with rapid response at 4 weeks of treatment for genotype 1 could achieve sustained viral response at 48 weeks of treatment, while those with complete response at 12 weeks of treatment would have a sustained viral response rate of 60-70% at 48 weeks of treatment, and those with viral load below the detection line at 24 weeks of treatment would have a sustained viral response rate of only 45%. Those with no decrease in viral load at 4 weeks of treatment or a decrease of less than 2 log at 12 weeks of treatment are unlikely to achieve a sustained response even after completing the course of treatment. Regardless of when a patient achieves a viral response, it is important to ensure an adequate course of treatment in order to minimize the relapse rate and maximize the sustained response rate. For genotype 2/3, a shorter course of treatment than 24 weeks often results in relapse for those with high HCV RNA load prior to treatment, although some studies have shortened the course to 16 weeks or even 12 weeks for those with RVR. For patients with genotype 1/4, except for those with rapid viral response or complete early response who can be treated as usual, for those with partial or slow response, HCV RNA load should be tested at 24 weeks of treatment, and for those with viral response at 24 weeks, the treatment course should be extended to 72 weeks. Some investigators have suggested that the course of therapy should continue for an additional 44 weeks after the first viral response is achieved. Although numerous clinical trials have shown that even with PEG-IFN in combination with ribavirin, sustained viral response rates, especially in genotype 1 patients, are mostly below 60%, the absolute majority of these clinical trials were conducted on a regimen-neutral basis, and in order to maximize efficacy, treatment must be individualized on a patient-by-patient basis. Although the guidelines state that treatment should be stopped in the absence of early response, it is more reasonable to understand that stopping is the method used, both the type and dose of interferon and the dose of ribavirin. If the treatment is changed, a viral response can often be obtained as well. For those who do not respond to standard (plain) interferon combined with ribavirin therapy, PEG-IFN and increased ribavirin dosage may be used instead; for those who do not respond to PEG-IFN combined with ribavirin therapy, the dose of PEG-IFN and the dose of ribavirin may be increased. Since sustained viral response to antiviral therapy for chronic hepatitis C is based on effective doses and adequate regimens, and interferon and ribavirin themselves have numerous side effects that sometimes make it difficult to maintain doses and regimens, patient compliance is often one of the important variables affecting efficacy. For those on therapeutic doses with significant side effects, treatment should first be directed at the side effects rather than mitigating them by lowering the dose, and excessive dose reductions often lead to treatment failure. In conclusion, antiviral therapy for chronic hepatitis C is still based on IFN in combination with ribavirin, although some investigators have added gentamicin for combination therapy for those who are not effective with interferon in combination with ribavirin, or various protease inhibitors that are now in clinical trials, to obtain a sustained viral response, it is necessary to build on the HCV-specific cellular immunity, interferon combined with ribavirin therapy is the cornerstone of antiviral therapy for chronic hepatitis C.