Hepatitis G

　　Hepatitis G virus (HGV) is a single-stranded positive-sense RNA virus, with a gene length of about 9.4 kb, possessing a large continuous, translational single open reading frame, encoding a polyprotein precursor with more than 2870 amino acid residues. Hepatitis G can be caused by the following factors:

　　1. Blood or blood products containing the virus.

　　2. Maternal-child transmission, possible transmission routes include infection during the process of delivery or postpartum breastfeeding.

　　3. Intravenous drug use.

　　4. Iatrogenic transmission.

　　5. Sexual contact transmission, tattoo transmission, and other contacts involving bodily fluid exchange can all lead to infection.

　　Recurrent hepatitis G (HGV) can often lead to chronic hepatitis and liver cirrhosis, which has a great impact on the health of patients.

　　1. Chronic hepatitis

　　Chronic hepatitis refers to the fact that most chronic hepatitis is caused by the long-term treatment of acute hepatitis G (HGV) that does not heal, with the course lasting over half a year, and then turning into chronic hepatitis. There are also many chronic hepatitis patients who become infected with hepatitis viruses and develop into chronic hepatitis without showing symptoms. Chronic hepatitis has strong infectivity.

　　2. Liver cirrhosis

　　Liver cirrhosis is a common chronic progressive liver disease, caused by long-term or repeated action of one or more etiologies, leading to diffuse liver damage. Pathologically, there is widespread necrosis of liver cells, nodular regeneration of residual liver cells, proliferation of connective tissue, and the formation of fibrous septa, resulting in the destruction of the lobular structure and the formation of false lobules, leading to the gradual deformation and hardening of the liver, and eventually developing into liver cirrhosis. Clinically, it is mainly manifested by liver function damage and portal hypertension, with involvement of multiple systems, and late complications often include upper gastrointestinal bleeding, hepatic encephalopathy, and secondary infection.

　　The clinical manifestations of hepatitis G (HGV) are similar to those of acute hepatitis and can also be epidemic in fulminant hepatitis. The clinical manifestations lack distinct specificity, with general symptoms and signs of viral hepatitis, such as anorexia, nausea, discomfort or pain in the upper right quadrant of the abdomen, jaundice, liver enlargement, and tenderness in the liver area. Hepatitis G (HGV) mainly has three subtypes:

　　1. GBV-c

　　It can be found in Africa, North America, Asia, and Europe.

　　2. New group

　　It is mainly found in Asia and Europe.

　　3. HGV

　　It is mainly found in Europe, Asia, and North America.

　　The main source of hepatitis G (HGV) infection is blood transfusion and the use of blood products, therefore, screening blood sources and blood products is a major measure for preventing HGV infection. This requires clear, rapid, and simple detection methods, and the reduction of contamination of blood products. In addition to preventing viral infection, attention should also be paid to daily life:

　　1. Vaccine

　　There is currently no satisfactory preventive vaccine for hepatitis G (HGV).

　　2. Abstaining from alcohol

　　Abstaining from alcohol is a major factor in protecting the liver.

　　3. Limiting fat intake

　　Prevention through diet control is possible, such as controlling the intake of sugary foods. In addition, exercise can be used to burn off excess body fat. For those who have already developed fatty liver, if they can control their diet and persist in physical exercise, they can consume body heat, control weight gain, and as obesity decreases, the fat in the liver will also diminish, liver function will return to normal, and no medication is needed.

　　Currently, the laboratory diagnosis of HGV infection mainly uses reverse transcriptase polymerase chain reaction (RT-PCR) to detect HGVRNA in serum and enzyme-linked immunosorbent assay (EIA) to detect anti-HGV antibodies in serum. Approximately one week after the human infection with hepatitis G virus, HGVRNA can be detected in serum, and anti-HGV antibodies usually appear positive after 3 weeks of infection. Therefore, RT-PCR can be used as an early diagnosis of HGV infection. According to foreign reports, the positive coincidence rate between EIA and RT-PCR is only 3% to 18%, and it is not suitable as a laboratory diagnosis of HGV infection. However, the positive coincidence rate between the self-developed anti-HGVEIA in China and RT-PCR can reach as high as 60%, and it is expected to be used for the screening of HGV infection.

　　HGV patients should choose healthy foods and beverages instead of high-fat, high-carbohydrate, and high-calorie foods in their diet. They should eat a variety of fresh vegetables and fruits, whole grains, and legumes, reduce the intake of fatty meat and animal fat, avoid eating processed meats, and avoid smoking and drinking. They should maintain a good mental state, avoid staying up late, have sufficient sleep, and engage in moderate exercise.

　　Due to the relatively short time of systematic research on hepatitis G virus (HGV) and the fact that the research is mainly concentrated on etiology, molecular biology, and epidemiology, clinical treatment still requires a relatively long period of efficacy observation to draw conclusions. In addition to general liver protection treatment, the research currently focuses more on interferon therapy. Some scholars have found cases of simultaneous HGV infection in chronic hepatitis C and B patients who have received interferon alpha (α-IFN) treatment. The research results show that the overlapping infection of HGV does not affect the response of hepatitis B or C to α-IFN, and the treatment of α-IFN during HGV infection is equally sensitive, but only a few patients continue to have negative viral conversion. Therefore, the dosage and course of IFN treatment should still be further explored in the future.