v 中

1. Hepatitis A: Hepatitis A is caused by Hepatitis A virus (HAV). The HAV particle is spherical, measuring 27–32 nm in diameter, without an envelope, possessing a 20-sided cubic symmetry and containing single-stranded RNA. HAV can be inactivated by heating at 100°C for 5 minutes, exposing to ultraviolet light for 1 hour, or treating with chlorine at a concentration of 1 mg/L for 30 minutes. Both rhesus monkeys and chimpanzees are susceptible to infection. Clinical samples can isolate HAV, but cell culture does not induce cytopathic effects. HAV exists in only one serotype and one antigen-antibody system; gM antibodies are present only within 12 weeks after onset, while IgG antibodies persist for a long time. The feces and blood of Hepatitis A patients are infectious, primarily transmitted orally; sporadic cases arise from everyday contact, while water and food contamination often lead to outbreaks. For example, in 1988, Shanghai experienced a major Hepatitis A epidemic caused by contaminated pork fat, infecting approximately 300,000 people. Hepatitis A is most common in children, with no chronic or asymptomatic carriers. Post-infection immunity is generally strong. In addition to hygiene measures, vaccination against Hepatitis A can prevent Hepatitis A.
2. Hepatitis B: Hepatitis B is caused by the Hepatitis B virus (HBV). HBV belongs to the family Hepadnaviridae, with a genome length of about 3.2 kb, consisting of partially double-stranded circular DNA. After HBV enters the human body, it binds to receptors on the hepatocyte membrane, sheds its envelope, and enters the hepatocyte cytoplasm. Once inside, HBV removes its capsid, allowing some of the double-stranded HBV DNA to enter the hepatocyte nucleus. Under the action of host enzymes, the negative-sense DNA serves as a template for extending the positive-sense strand, repairing gaps in the positive-sense strand, forming covalently closed circular DNA (cccDNA). Then, using cccDNA as a template, HBV transcribes several different-length mRNAs under the influence of host RNA polymerase II, among which the 3.5-kb mRNA contains all the genetic information of HBV-DNA, known as the pre-genomic RNA. The latter enters the hepatocyte cytoplasm as a template, where HBV reverse transcriptase synthesizes negative-sense DNA; then, using negative-sense DNA as a template, HBV DNA polymerase synthesizes positive-sense DNA, forming partial double-stranded DNA, which eventually assembles into complete HBV and is released outside the hepatocyte. The daughter double-stranded DNA in the cytoplasm can also enter the hepatocyte nucleus, where it forms cccDNA and continues replication. The half-life of cccDNA is long, making it difficult to completely eliminate from the body. Based on differences in the full HBV genome sequence or the S-region gene sequence, HBV can be divided into eight genotypes, A through H8. Each genotype further subdivides into different subgenotypes. Different genotypes respond differently to antiviral therapies. During antiviral treatment, HBV genotypes are prone to mutation, leading to drug resistance and complicating treatment. The HBV antigen-antibody system includes HBsAg and anti-HBs, HBcAg and anti-HBc, HBeAg and anti-HBe. HBsAg is present in the blood and various bodily fluids of infected individuals and asymptomatic carriers, serving as an indirect indicator of HBV presence. Anti-HBs are protective antibodies; when these antibodies appear in the blood after infection or vaccination, it signifies that the individual has acquired immune protection. HBcAg is mainly located in the hepatocyte nucleus, typically absent in peripheral blood; anti-HBc exists in two forms—IgM and IgG—in the blood. The former indicates active infection, while the latter reflects past infection. HBeAg, together with HBV-DNA and DNA-P, are key indicators of HBV replication and infectivity; anti-HBe appears in the blood as HBeAg disappears, indicating reduced HBV replication and decreased infectivity. Regularly monitoring the above HBV markers in the blood (HBV-M) can help assess the level of infectivity, disease progression, and prognosis. HBV is highly resistant to environmental factors; it can be inactivated by heating at 65°C for 10 hours, boiling for 10 minutes, or sterilizing with high-pressure steam. Chlorine-based agents, ethylene oxide, glutaraldehyde, peracetic acid, and iodophor also demonstrate good inactivation effects. HBV infection is widespread globally, though the prevalence varies significantly across regions. According to the World Health Organization, approximately 2 billion people worldwide have been infected with HBV, among whom 350 million are chronic HBV carriers. Each year, around 1 million people die from liver failure, cirrhosis, and primary hepatic carcinoma (HCC) caused by HBV infection. China is a region with a high prevalence of HBV infection, with a HBsAg positivity rate of about 9% among the general population. The HBsAg positivity rates among vaccinated and unvaccinated individuals were 4.51% and 9.51%, respectively. The main HBV serotypes prevalent in China are adw2 and adrq+, while the predominant genotypes are C and B. HBV is primarily transmitted through blood and blood products, mother-to-child transmission, broken skin and mucous membranes, and sexual contact. Mother-to-child transmission is a major mode of transmission in China, with infants often contracting HBV through exposure to the blood and bodily fluids of HBV-positive mothers at birth. Skin and mucous membrane transmission occurs mainly through the use of improperly sterilized medical instruments, syringes, invasive diagnostic and therapeutic procedures, and surgical operations, as well as through intravenous drug abuse. Other modes of transmission include foot care, tattooing, ear piercing, accidental exposure during medical procedures, sharing razors and toothbrushes, and other similar practices. Sexual contact with HBV-positive individuals—especially those with multiple sexual partners—increases the risk of HBV infection significantly. Thanks to strict HBsAg screening programs for blood donors, HBV infections caused by blood transfusions or blood products have become less common. However, routine work or everyday contact—such as handshakes, hugs, living in the same dormitory, dining in the same restaurant, or sharing toilets—without direct blood exposure generally do not transmit HBV. Transmission via mosquitoes, bedbugs, and other blood-sucking insects has not been confirmed. Vaccination against HBV is the only effective method for preventing HBV infection and is now included in national immunization programs. When HBV infects a person, if the virus persists for 6 months without being cleared, the condition is considered chronic HBV carriage. The age at infection is the primary factor influencing whether the infection becomes chronic. The vertical transmission rate from mother to child is 90%, while infants infected in early childhood have a 25–30% chance of becoming chronic, whereas adolescents and adults only have a 5–10% chance of developing chronic infection. After HBV infection, the disease typically progresses through three phases: the immune tolerance phase, the immune clearance phase, and the inactive or low-replication phase. Many chronic HBV carriers, after a certain period, experience recurrent episodes of disease progression, with significant liver damage and even liver failure. The incidence of liver cirrhosis and HCC increases to 23% and 4.4%, respectively.
3. Hepatitis C: Hepatitis C is caused by the Hepatitis C virus (HCV). HCV belongs to the Flaviviridae family, with a size of 50–60 nm, and its outer shell contains lipids. Its genome is single-stranded positive-sense RNA, highly mutable; currently, it can be divided into six genotypes and different subtypes. Following international standards, HCV genotypes are represented by Arabic numerals, while gene subtypes are indicated by lowercase English letters (e.g., 1a, 2b, 3c, etc.). Genotype 1 is globally distributed, accounting for over 70% of all HCV infections. After HCV infection, a certain period allows the infected individual to develop a viral population dominated by a single dominant strain, known as quasispecies. The HCV genome contains an open reading frame (ORF) that encodes more than ten structural and non-structural proteins; NS3 protein is a multifunctional protein with protease activity at its amino terminus, and... v 中 水 未 数 he 及 鲁 业,

羧基端 possesses helicase/tri-phosphate nucleoside enzyme activity; NS5B protein is an RNA-dependent RNA polymerase, both essential for HCV replication and critical targets for antiviral therapy. HCV is sensitive to common chemical disinfectants; heating at 100°C for 5 minutes, or at 60°C for 10 hours, as well as high-pressure steam and formaldehyde fumigation, can all inactivate the virus. Hepatitis C is globally prevalent and is a leading cause of end-stage liver disease in Europe, America, Japan, and other countries. The global HCV infection rate is approximately 3%. Epidemiological surveys in China show that the anti-HCV positivity rate among the general population is 3.2%, with no significant difference between men and women. The main HCV genotype is 1b, followed by 2a, while other genotypes are relatively rare. Hepatitis C is primarily transmitted through blood, such as through the transfusion of blood and blood products, or via broken skin and mucous membranes—through intravenous drug use, the use of non-disposable syringes and needles, sharing razors, toothbrushes, tattooing, and ear piercing. Sexual transmission is also an important route of HCV spread, and mother-to-child transmission can occur, though the transmission routes of some HCV-infected individuals remain unknown. Kissing, hugging, sneezing, coughing, eating, drinking from shared utensils and cups, and other contact without skin breaks or blood exposure generally do not transmit HCV. Like Hepatitis B, Hepatitis C is prone to becoming chronic and is a major cause of liver cirrhosis and liver cancer. The markers of infection in the blood include anti-HCV and HCV-RNA positivity. Vaccines are currently under development. 4. Hepatitis D: Hepatitis D is caused by the Hepatitis D virus (HDV), also known as the Hepatitis Delta virus. HDV is a subviral pathogen associated with HBV, causing both acute and chronic hepatitis. HDV is a member of the Arenaviridae family, specifically the deltavirus genus. Mature HDV is spherical, with a diameter of 35–37 nm, and its viral particles contain ribonucleoproteins composed of viral genomes and antigens, with the envelope being HBsAg. HDV is a defective virus that requires assistance from HBV or other hepatotropic viruses to replicate. The routes of infection and preventive measures are similar to those for Hepatitis B; vaccines have not yet been successfully developed. 5. Hepatitis E: Hepatitis E is caused by the Hepatitis E virus (HEV). HEV is a 32–34 nm RNA virus, transmitted via the fecal-oral route, often resulting in large-scale outbreaks due to fecal contamination of drinking water sources. Its clinical and epidemiological characteristics are similar to those of Hepatitis A. From 1986 to 1988, a major Hepatitis E outbreak occurred in southern Xinjiang, China, caused by water source contamination, affecting nearly 120,000 people. Hepatitis E vaccines have not yet been developed. 6. Hepatitis G: Hepatitis G is caused by the Hepatitis G virus (HGV). HGV is also known as GBV-C.

<!-- translated-chunk:36/261 -->

Task output rules: Translate this markdown block from Chinese to English. Preserve markdown markers, links, and formatting. Keep headings and list structure unchanged. Return only the translated block.

Input: Fragrant herbs, thick-bark, sea sandalwood, plantain seeds). Heat-toxin internal infiltration is often associated with severe hepatitis, primarily treated by clearing heat and detoxifying, transforming turbidity and opening up the orifices, using Yin Chen Hao Tang combined with Shen Xi Dan with modifications (Yin Chen, Zhizi, Xijiao, Dahuang, Huangqin, Lianqiao, Jin Yin Hua, Changpu, Yujin, Banlan Gen, Zicao, Shengdi, Xuan Shen, Longdan). Liver Qi stagnation type is commonly seen in non-jaundice hepatitis and some cases of prolonged hepatitis. Treatment focuses on soothing the liver and resolving stagnation, harmonizing the stomach and regulating qi. Chai Hu Shu Gan San with modifications (Chai Hu, Bai Shao, Zhi Ke, Dan Shen, Chao Xiang Fu, Yujin, Fu Ling, Gan Cao) is used. Liver and kidney yin deficiency type is often observed in prolonged or chronic hepatitis, or in cases where there is a tendency toward early liver cirrhosis; treatment emphasizes nourishing yin and softening the liver. Yidun Jian with modifications (Shashen, Shengdi, Dang Gui, Gou Qi Zi, Jin Ling Zi, Dan Shen, Mai Dong, Bai Shao, Shan Yao, Gu Ya) is employed. During the recovery phase of acute hepatitis and in cases of chronic hepatitis, symptoms of spleen-stomach dysfunction are common. Treatment focuses on strengthening the spleen and replenishing qi, as well as harmonizing the liver and regulating the stomach, using Shen Ling Zhu Cao Tang with additions and subtractions (Sha Ren, Mu Xiang, Ji Nei Jin, Fu Ling, Pao Shen, Mai Ya, Dan Shen, Bai Zhu, Shan Yao, Gu Ya). (China Practical Medicine, 2006.9)

Ma Yongcai treated 86 cases of chronic type B hepatitis using the Eight Methods for Removing Dampness, achieving significant results in 42 cases, improving in 44 cases, with an overall effective rate of 100%.