1. Hepatitis C transmission route 1. HCV is mainly transmitted by blood, mainly: (1) transmitted by blood transfusion and blood products. This route has been effectively controlled since 1993 when blood donors were screened for anti-HCV. However, due to the window period of anti-HCV, the unstable quality of anti-HCV testing reagents and the fact that a small number of infected patients do not produce anti-HCV, it is not possible to completely screen out HCV RN A-positive people, and there is still a possibility of HCV infection from massive blood transfusion and hemodialysis.(2) Transmission via broken skin and mucous membrane. This is by far the predominant mode of transmission, with HCV transmission due to intravenous drug use accounting for 60% to 9 0% in some areas. The use of non-disposable syringes and needles, non-sterile dental instruments, endoscopy, invasive procedures and needlesticks are also important routes of transmission through the skin and mucous membranes. Some traditional medical practices that may lead to skin breakdown and blood exposure are also associated with HCV transmission; sharing razors, toothbrushes, tattoos, and ear piercing are also potential modes of HCV transmission via blood. 2. Sexual transmission: People who have sexual intercourse with HCV-infected persons and those who have sexual promiscuity have a higher risk of contracting HCV. People with other sexually transmitted diseases, especially those infected with human immunodeficiency virus (HIV), are at higher risk of HCV infection. The risk of mother-to-child transmission: The risk of HCV transmission from an anti-HCV-positive mother to her newborn is 2%, but if the mother is positive for HCV RNA at the time of delivery, the risk of transmission can be as high as 4% to 7%; the risk of transmission increases to 20% when HIV infection is combined. The route of transmission for some HCV-infected patients is unknown. The natural history of hepatitis C is that HCV RNA can be detected in peripheral blood 1 to 3 weeks after exposure to HCV, but only 50% to 70% of patients are anti-HCV positive at the time of clinical symptoms in acute HCV infected patients, and about 90% of patients are anti-HCV positive after 3 months. However, only 50-70% of patients with acute HCV infection are anti-HCV positive at the time of clinical symptoms, and about 90% of patients are anti-HCV positive after 3 months. After HCV infection, viraemia persists for 6 months without clearance and the chronicity rate of hepatitis C is 50%-85%. The incidence of cirrhosis 20 years after infection is 2%-4% in children and young women, 20%-30% in middle-aged patients infected by blood transfusion, and 10%-15% in the general population; the rate of spontaneous clearance of HCV infection is higher in people under 40 years of age and in women; HCV infection in men over 40 years of age and co-infection with HIV that leads to immunocompromise can contribute to disease progression. Co-infection with hepatitis B virus (HBV), alcoholism (50 g/d or more), non-alcoholic fatty liver disease (NASH), high iron load in the liver, co-infection with schistosomes, hepatotoxic drugs, and toxic substances from environmental pollution may also contribute to disease progression. The incidence of HCV-associated HCC ranges from 1% to 3% after 30 years of infection, mainly in patients with cirrhosis and progressive liver fibrosis, and once cirrhosis has developed, the annual incidence of HCC is 1% to 7%. The above factors that promote the progression of hepatitis C, as well as diabetes, can contribute to the development of HCC. The incidence of HCC is relatively high in patients with hepatitis C after blood transfusion. The quality of life of patients with cirrhosis and HCC is reduced. Cirrhosis and HCC are the leading causes of death in patients with chronic hepatitis C, with decompensated cirrhosis being the most predominant. The 10-year survival rate has been reported to be about 80% once cirrhosis occurs and only 25% if decompensation occurs. The incidence of HCC is lower in complete responders (including relapsers after complete response) after interferon (IFN) α therapy, but higher in non-responders. (a) Hepatitis C vaccine prevention There is no effective vaccine to prevent hepatitis C. (2) Strict screening of blood donors Strictly implement the Blood Donation Law of the People’s Republic of China and promote blood donation without compensation. Strictly screen blood donors by testing serum anti-HCV and alanine aminotransferase (ALT). The detection of HCV antigen should be developed to improve the detection rate of window stage infected patients. (iii) Prevention of transdermal and mucosal transmission Promote safe injections. Medical instruments such as dental instruments and endoscopes should be strictly sterilized. Medical personnel should wear gloves when touching patients’ blood and body fluids. Provide psychological counseling and safety education to intravenous drug users to persuade them to quit drugs. Do not share razors, dental instruments, etc. Haircutting tools, piercing and tattooing tools should be strictly disinfected. (iv) Prevention of sexual transmission Those with a history of sexual promiscuity should be examined regularly and management should be strengthened. It is recommended that HCV-infected persons use condoms during sexual intercourse. Proper sex education should be provided to adolescents. （Pregnant women who are positive for HCV RNA should avoid amniocentesis, minimize the time of delivery, ensure the integrity of the placenta, and reduce the exposure of the newborn to maternal blood. Clinical diagnosis of hepatitis C. Treatment of general hepatitis C patients 1. Acute hepatitis C: IFNα therapy significantly reduces the chronicity of acute hepatitis C. Therefore, antiviral therapy should be started if HCV RNA is detected. There is no unified protocol for the treatment of acute hepatitis C. It is recommended that common IFNα 3MU be given by intramuscular or subcutaneous injection every other day for 24 weeks, and ribavirin 800-1000 mg/d should be taken concurrently. 2. Chronic hepatitis C: (1) persistent or recurrent elevation of ALT or AST, or liver histology with significant inflammatory necrosis (G≥2) or moderate fibrosis (S≥2) Those who are prone to progression to cirrhosis should be given active treatment. (2) Most people with persistently normal ALT have mild liver lesions and should be treated or not based on the pathological findings of liver biopsy. For those with significant fibrosis (S2, S3), antiviral therapy should be given regardless of the degree of inflammatory necrosis; for those with mild inflammatory necrosis and no significant fibrosis (S0, S1), treatment can be withheld, but liver function should be tested every 3 to 6 months. (3) ALT levels are not an important predictor of patient response to IFNα. It has been previously reported that treatment of hepatitis C patients with normal ALT with generic IFNα has no significant effect, and therefore IFNα therapy is not recommended. However, a recent study found that the virological response rate of hepatitis C patients with normal ALT treated with PEG-IFNα-2a in combination with ribavirin was similar to that of hepatitis C patients with elevated ALT. Therefore, patients with normal or mildly elevated ALT can be treated as long as they are positive for HCV RNA, but more cases need to be accumulated for further study. 3. Hepatitis C cirrhosis: (1) Patients with compensated cirrhosis (Child-Pugh class A) are recommended to be given antiviral therapy under close observation in order to stabilize the disease and delay or prevent complications such as liver failure and HCC, although the tolerance and efficacy of treatment are reduced. (2) Patients with decompensated cirrhosis have difficulty tolerating the adverse effects of IFNα therapy and should undergo liver transplantation if available. 4. Hepatitis C relapse after liver transplantation: Patients with HCV-related cirrhosis or HCC have a high rate of recurrence of HCV infection after liver transplantation; IFNα therapy has some effect on such patients, but it may promote rejection of the transplanted liver, and antiviral therapy can be administered under the guidance and close observation of experienced specialists. The treatment of patients with special hepatitis C. 1. Children and the elderly: Experience with the treatment of chronic hepatitis C in children is inadequate. In principle, antiviral therapy should be administered to elderly patients aged 65 or 70 years or older, but it is generally less well tolerated. Therefore, the decision to administer antiviral therapy should be based on a comprehensive assessment of the patient’s age, drug tolerance, comorbidities (e.g., hypertension, coronary artery disease), and the patient’s wishes. 2. Alcohol and drug addicts: Chronic alcoholism and drug addiction may promote HCV replication and aggravate liver damage, thus accelerating the process of developing cirrhosis or even HCC. Because of the low compliance, tolerance and SVR rate of antiviral therapy in alcohol and drug addicts, treatment of hepatitis C must be accompanied by alcohol and drug abstinence. 3. Combined HBV or HIV infection: Combined HBV infection accelerates the progression of chronic hepatitis C to cirrhosis or HCC. For those with positive HCV RNA and negative HBV DNA, anti-HCV therapy should be given first. For those with active replication of both viruses, IFNα plus ribavirin is recommended to clear HCV first, and then anti-HBV therapy can be given to those with persistent positive HBV DNA after treatment. The treatment of these patients requires further study to determine the best treatment regimen. Combined HIV infection can also accelerate the progression of chronic hepatitis C. Anti-HCV therapy depends on the patient’s CD4+ cell count and the stage of fibrosis in the liver tissue. Patients who are immunocompetent and have no immediate indication for highly active antiretroviral therapy (HAART) should be treated first for HCV infection; patients on HAART with S2 or S3 liver fibrosis should be given concurrent anti-HCV therapy; however, special attention should be paid to the possibility of interaction between ribavirin and anti-HIV nucleoside analogs, including lactic acidosis. For patients with severe immunosuppression (CD4+ positive lymphocytes <2×108/L), anti-HCV therapy should be given first, and anti-HCV therapy should be considered after the immune function is reestablished. 4. Chronic renal failure: For chronic hepatitis C with renal failure and not on dialysis, antiviral therapy should not be administered. Patients who are on dialysis and do not have histopathologic cirrhosis (especially in preparation for renal transplantation) may be treated with IFNα alone (care should be taken to administer it after dialysis). Ribavirin combination therapy is generally not indicated because of the risk of severe hemolysis in patients with renal insufficiency. HCV RNA genotyping (type 1 and non-type 1) and quantification of HCV RNA in blood should be performed prior to treatment to determine the course of antiviral therapy and the dose of ribavirin. For patients with HCV RNA genotype 1 or HCV RNA quantification ≥2×106 copies/ml, one of the following regimens may be used: 1. PEG-IFNα combined with ribavirin regimen 2. For patients who relapsed after initial IFNα treatment alone, a high SVR rate (47%, 60%) was achieved with PEG-IFNα-2a or regular IFNα combined with ribavirin; for patients who did not respond to initial IFNα alone, the SVR rate was lower with regular IFNα or PEG-IFNα-2a combined with ribavirin (12%-15% and 34%-40%, respectively). 40%). PEG-IFNα-2a in combination with ribavirin can be tried in patients who do not respond to initial combination therapy with regular IFNα and ribavirin or who relapse.