Viral hepatitis is a disease caused by infection with hepatitis viruses. Five types of hepatitis viruses have been identified: hepatitis A virus, hepatitis B virus, hepatitis C virus, hepatitis D virus and hepatitis E virus. The hepatitis A virus HAV is a member of the small ribonucleic acid virus family and is a hepatophilic RNA virus. It can survive for 30 days at 25°C in dry feces and for months in shellfish, sewage, fresh water, seawater, and mud. This stability is very favorable for HAV transmission through water and food. High-pressure steam (121°C, 20 minutes), boiling for five minutes, UV irradiation, formalin (1:4000, 37°C for 72 hours), potassium permanganate (30mg/L, 5 minutes), iodine (3mg/L, 5 minutes), chlorine (free chlorine 2.0-2.5mg/L, 15 minutes), and 70% alcohol at 25°C for 3 minutes are effective in inactivating HAV. Hepatitis B virus ( HBV belongs to the family of hepatophilic DNA viruses (hepadnaviridae), with a genome length of about 3.2 kb and partially double-stranded cyclic DNA. HBV is more resistant, but HBV can be inactivated by 65°C for 10 h, boiling for 10 min or high-pressure steam. ethylene oxide, glutaraldehyde, peroxyacetic acid and iodine volts also have a good inactivation effect on HBV. after HBV invades hepatocytes, the Part of the double-stranded circular HBV DNA is used in the nucleus as a template to extend the positive strand to repair the gap area in the positive strand, forming covalent closed circular DNA (cccDNA); then cccDNA is used as a template to transcribe into several different lengths of mRNA, which are used as pre-genomic RNA and encode various antigens of HBV. cccDNA has a long half-life (life) and is difficult to be completely removed from the body. It is difficult to completely remove from the body. Hepatitis C virus is an RNA virus (HCVRNA) that is currently classified into six different genotypes and subtypes, such as 1a, 2b, 3c, etc. Genotype 1 is globally distributed and accounts for more than 70% of all HCV infections. Hepatitis C virus is sensitive to general chemical disinfectants, and high temperature heating and formaldehyde fumigation can inactivate the virus. Hepatitis D virus (HDV) is a defective virus that depends on hepatitis B virus for the completion of its biological cycle, so hepatitis D cannot exist alone and must be present in the presence of HBV to infect and cause disease. the HDV genome is a single-stranded RNA that forms a viral particle with a complete structure, 35-37 nm in diameter, whose outer shell is the hepatitis B surface antigen HBsAg, internal by HDAg and HDV-RNA knot, and HDV-RNA and HBV-DNA no homology, nor is the host RNA, but the genome of HDV, currently known HDV only a serotype, but HDV is prone to mutation, mutation produced by different strains of virulence vary, most scholars now believe that HDV infection can significantly inhibit HBV -DNA synthesis. Hepatitis E virus is a single-stranded positive-stranded RNA virus, about 7.5 kb long, with a symmetrical icosahedral appearance, no shell, 32-34 nm in diameter, and surface structures with protrusions and indentations (Indentations). It used to be classified in the family Cupaviridae, but now it is classified in the family Hepatitis viruses. The virus has two major strains, the Burmese (or Asian) and Mexican strains. HEV is unstable, sensitive to high salt, cesium chloride, chloroform, and has reduced activity in repeated freeze-thaw (between -70°C and 8°C) and in sucrose solution, but is more stable in alkaline environments Diagnosis and differential diagnosis: The diagnosis of viral hepatitis is based on the clinical manifestations of hepatitis combined with epidemiological history, and detection of virus-specific markers. The marker for the diagnosis of hepatitis A is a positive anti-HAVIgM, which is usually detected in the serum about 1 week after the onset of the disease. The markers for confirming the diagnosis of hepatitis B are positive for at least 2-3 of the five hepatitis B items (HBsAg, anti-HBs, HBeAg, anti-HBe, anti-HBc) (major triplet: HBsAg, HBeAg, anti-HBc or minor triplet: HBsAg, anti-HBe, anti-HBc), the load of hepatitis B HBV DNA can reflect the active level of viral The marker for confirming the diagnosis of hepatitis C is anti-HCV positivity; the marker for confirming the diagnosis of hepatitis E is anti-HEVIgM anti-HEV positivity; the marker for confirming the diagnosis of hepatitis D is anti-HDV positivity or HDV antigen positivity. Viral hepatitis needs to be differentiated from hemolytic jaundice, extrahepatic obstructive jaundice, hepatitis due to non-hepatophilic viruses (e.g. cytomegalovirus, EBV), drug-induced liver damage, alcoholic liver disease, autoimmune hepatitis, and other diseases. Treatment prognosis: Treatment of viral hepatitis A and E does not require antiviral therapy, but mainly supportive therapy, supplemented by appropriate liver-protective drugs such as glycopyrrolate preparations, silymarin, reduced glutathione, polyenyl phosphatidylcholine, etc. Avoid alcohol, fatigue, and liver-damaging drugs. Emphasis on early bed rest, until the symptoms are significantly reduced, can gradually increase the activity, in order not to feel fatigue as the principle, need to be hospitalized in isolation until 3 weeks after the onset of the disease, clinical symptoms disappeared, serum total bilirubin in 17.1umol/L or less, ALT in the normal value of 2 times or less can be discharged, but after discharge should still rest 1-3 months, after resuming work should be regularly re-examined six months – 1 year. The treatment of acute hepatitis B is basically the same as above, as to whether to carry out antiviral therapy needs to be determined according to the patient’s HBV DNA and hepatitis B five serological conversion, chronic viral hepatitis B, if with the indications for antiviral therapy, in the above-mentioned liver preservation treatment based on the need for antiviral therapy. China’s 2012 guidelines for the prevention and treatment of hepatitis B indications for antiviral treatment of hepatitis B are: HBeAg positive, HBV-DNAR 20000IU/ml; HBeAg negative, HBV-DNAR 2000IU/ml; ② ALTR2×ULN; if treated with IFN, ALT should be Q10×ULN and total serum bilirubin should be 2×ULN; ③ ALT2×ULN, but liver histology shows KnodellHAIR4, or inflammatory necrosis RG2, or fibrosis RS2. Antiviral therapy should also be considered for those who are persistently HBV-DNA positive and do not meet the above treatment criteria, but have one of the following conditions: ① for those with ALT greater than ULN and aged 40 years, antiviral therapy should also be considered; ② for those with persistently normal ALT but If liver histology shows KnodellHAIR4, or inflammatory necrosis RG2, or fibrosis RS2, antiviral therapy should be given actively; ③ If dynamic observation reveals evidence of disease progression (e.g. enlarged spleen), liver histology is recommended and antiviral therapy should be given if necessary. Anti-viral therapy for hepatitis B includes common interferon, pegylated interferon and nucleoside (acid) analogues (including lamivudine, adefovir, telbivudine, entecavir and tenofovir). Interferon analogs have a relatively slow onset of action, but have a relatively high chance of maintaining stable efficacy and a relatively short course of treatment, with the disadvantage of having more side effects; nucleoside (acid) analogs have a fast onset of action and fewer side effects, but have a longer course of treatment and a higher chance of relapse after stopping the drug. Therefore, it is necessary to select the drug according to the patient’s specific situation, and to adjust the program according to the patient’s response during the treatment process for individualized treatment. If nucleoside (acid) analogs are chosen for treatment, attention should also be paid to the possibility of viral resistance mutations. Viral hepatitis C, whether acute or chronic, requires antiviral therapy as long as HCV RNA is detectable. The standard antiviral regimen is pegylated interferon plus ribavirin or, if pegylated interferon is not economically feasible, plain interferon may be substituted, with the duration of therapy determined by the patient’s response at 4, 12, and 24 weeks of treatment (i.e., response-guided therapy – RGT therapy). Direct-acting antivirals such as boceprevir (BOC) or telaprevir (TVR) may also be considered for patients with genotype 1 who have a poor response. The prognosis for different types of viral hepatitis varies. Hepatitis A is predominantly acute hepatitis without chronicity and has a good prognosis. The incidence of severe hepatitis is about 0.2-0.4% of all cases of hepatitis A. The morbidity and mortality rate is high. Those who have had hepatitis A or latent infection can acquire lasting immunity. The prognosis for most hepatitis E is good. Most recover in 1-4 weeks, and no cases of chronic hepatitis or cirrhosis have been found. A small percentage of patients with concomitant cholestasis may have a longer course. Acute hepatitis B infected in adulthood mostly recovers completely, and a few will turn into chronic hepatitis, while hepatitis B infected in infancy and early childhood often turns chronic and goes through immune tolerance, immune clearance, inactive and reactive phases, and some patients may develop cirrhosis or liver cancer. Chronic hepatitis C can be cured by active antiviral treatment, but untreated patients may develop cirrhosis or liver cancer. Preventive care: The prognosis of different types of viral hepatitis is different. Hepatitis A is predominantly acute, non-chronic and has a good prognosis. The incidence of severe hepatitis accounts for about 0.2-0.4% of all hepatitis A cases and has a high mortality rate. Those who have had hepatitis A or latent infection can acquire lasting immunity. The prognosis for most hepatitis E is good. Most recover in 1-4 weeks, and no cases of chronic hepatitis or cirrhosis have been found. A small percentage of patients with concomitant cholestasis may have a longer course. Acute hepatitis B infected in adulthood mostly recovers completely, and a few will turn into chronic hepatitis, while hepatitis B infected in infancy and early childhood often turns chronic and goes through immune tolerance, immune clearance, inactive and reactive phases, and some patients may develop cirrhosis or liver cancer. Chronic hepatitis C can be cured by aggressive antiviral therapy, but untreated patients may develop cirrhosis or liver cancer. Therefore, patients with chronic hepatitis B and C need to pay attention to the disease, long-term review and follow-up testing under the guidance of doctors, and manage the disease well, there will be a good outcome.