Childhood hepatitis D virus infection

　　1. Etiology

　　The complete HDV particle is spherical, with a diameter of 35-37 nm, containing HDV RNA and HDAg, and its capsid is HBsAg. HDV RNA is the genome of HDV, consisting of 1679-1683 nucleotides, forming a single-stranded, circular structure, and can be folded into a non-branching rod-like structure. HDV-RNA has 9 coding regions (ORFs), and ORF5 can encode HDAg. HDAg is a nuclear protein that can induce the body to produce anti-HDIgM and anti-HDIgG. Anti-HDIgM appears earlier, usually positive in the early stage of acute HDV infection, and gradually disappears in the convalescent period. A persistently high titer of anti-HDIgM suggests chronicization of the disease. Anti-HDIgG appears later, usually appearing 3-8 weeks after onset and can remain positive for many years at a low titer. When the disease is active, anti-HDIgG levels increase. The current infection often shows a positive anti-HDIgM, while past infection shows a negative anti-HDIgM but a positive anti-HDIgG. Anti-HD is not a neutralizing antibody, and infection can still be present when positive.

　　HDV infection can significantly inhibit the synthesis of HBV DNA. Serological tests prove that the appearance of HDAg is consistent with the decrease of HBV DNA in serum, and HBV DNA decreases when HDAg expression increases. When HDAg expression is at its peak, HBV DNA is often absent, but it recovers to the original level with the appearance of HDAg-negative and anti-HD. It was previously believed that the assembly of HDV depends on the synthesis of HBsAg, and its replication and expression also require assistance from HBV or other hepatotropic viruses. In vitro transfection experiments have shown that the replication of HDV-RNA and the expression of HDAg do not require the assistance of hepatotropic viruses, and HDV can complete independently, but a complete HDV must be formed by providing the capsid by hepatotropic viruses.

　　2. Pathogenesis

　　The pathogenesis of hepatitis D is not yet clear, and it is very likely that there is both the direct pathogenic effect of HDV and the host immune response mediated.

　　HDV may use the same mechanism as HBV, using the liver cell receptors present in the liver cells that contain HBsAg in the Pre-S1 protein and Pre-S2 protein of the shell to infect liver cells. Immunopathological findings show that HDAg-positive liver cells have varying degrees of lesions; in situ hybridization shows that HDV RNA in liver cells is distributed in areas with more obvious liver cell lesions; some people have used HDAg recombinant plasmids to transfect HepG2 liver cell line for culture, and a large amount of HDAg expression was observed in a short period of time, followed by necrosis of the cell line transfected. These experimental results indicate that HDV has a strong direct cytotoxic effect. Clinical data also show that asymptomatic carriers without obvious liver lesions can be found in patients with co-infection of HDV and HBV; in the liver tissue of HDV infection, inflammatory cells can be seen in the portal area, and lymphocytes infiltrate the liver parenchyma and extend pseudopods into liver cells. HDAg may be the target antigen attacked by the immune response. These also suggest that it is related to immune reactions.

　　1. Vitamin deficiency syndrome

　　Chronic hepatitis often has a vitamin D deficiency, and secondary to this, there is a lack of calcium and phosphorus, leading to osteomalacia, bone pain, and even fractures. Chronic hepatitis, liver cirrhosis, liver cancer, etc., often have a deficiency of vitamin A, leading to dark adaptation disorders and visual recovery disorders after bright light flickering. It can also occur in patients with a long course of acute hepatitis.

　　2. Dryness syndrome

　　Including dry keratitis, oral dryness, and a connective tissue disease (the most common being rheumatoid arthritis or systemic lupus erythematosus, in which the salivary glands or lacrimal glands may swell, more common in women aged 40-65, with a male-to-female ratio of 1:9, rare in children.)

　　3. Changes in thyroid function

　　The main occurrence is thyroid dysfunction, with increased serum protein-bound iodine and basal metabolic rate, and reduced iodine absorption. It is often caused by acute type A viral hepatitis.

　　1. Simultaneous infection with HDV and HBV

　　The incubation period is 6 to 12 weeks, and it is often manifested as acute jaundice. ALT can show a bimodal pattern. Due to the mutual restriction of the two viruses, the disease often presents as self-limiting with a good prognosis.

　　2. Co-infection with HDV and HBV

　　The incubation period is 3 to 4 weeks, and the clinical manifestations are related to the original HBV infection status. The general trend is that the original liver condition worsens, and asymptomatic HBsAg carriers often manifest as acute hepatitis or develop into chronic hepatitis; those with chronic hepatitis may worsen and are prone to develop acute or subacute fulminant hepatitis.

　　Currently, there is no hepatitis D vaccine. Since the hepatitis D virus is a defective virus, it must depend on the hepatitis B virus to replicate. Preventing hepatitis B virus infection can also prevent HDV infection, which is an effective means to control HDV infection. Widespread vaccination of hepatitis B vaccine for susceptible individuals can achieve the goal of preventing HDV infection. For those with HBsAg positivity who are reinfected with HDV, it is necessary to minimize blood transfusions, avoid or use less blood products, strictly screen blood donors and medical equipment for disinfection management to reduce the spread of HDV. With the research on new vaccines, the improvement of existing hepatitis B gene vaccines can prevent both HBV and HDV infections, and nucleic acid vaccines for the prevention of HDV will undoubtedly be available for immunoprophylaxis in the near future.

　　1. HDV Ag examination

　　The presence of HDV Ag in serum is a direct evidence for the diagnosis of acute infection. During acute hepatitis, the duration of viremia is on average 21 days, and the detection rate is 87% and 100% by ELISA and RIA, respectively. During chronic infection, the antigen persists but mostly in the form of immune complexes, requiring analysis by immunoblotting. The detection of HDV Ag in the liver has a higher direct diagnostic value.

　　2. AntihdV measurement

　　Antihdvi IgM appears in the early acute phase, maintains a high level during the chronic infection phase, and quickly decreases once the virus is eliminated; antihdvi IgG appears at a low level more than 3 to 8 weeks after onset; during chronic infection, it maintains a high concentration.

　　3. HDV RNA examination

　　The detection of HDV RNA in serum or liver tissue by dot hybridization or RT-PCR is a reliable indicator for the diagnosis of HDV infection.

　　First, therapeutic diet for hepatitis D

　　1. Augmented artemisia porridge

　　30 to 60 grams of artemisia, 6 grams of cyperus rotundus, appropriate amount of sugar, and 100 grams of glutinous rice. Grind cyperus rotundus into powder, first decoct artemisia to extract the juice and remove the dregs, then cook the glutinous rice with the clean glutinous rice, add the powdered cyperus rotundus after boiling, and finally add sugar to taste. Take twice a day, served warm.

　　2. Stewed bean curd with minced meat and winter mushrooms

　　100 grams of winter mushrooms, 100 grams of minced meat, 500 grams of tofu, 10 grams of scallion, 5 grams of ginger, 2 grams of cooking wine, 100 milliliters of meat broth, 2 grams of pepper powder, 5 grams of table salt, 5 grams of soy sauce, 20 grams of fresh peas, and 500 grams of vegetable oil (50 grams used). Cut the tofu into small cubes, fry in hot oil until golden brown and remove; heat a wok, add oil and stir-fry the minced meat, add scallion and ginger, then add cooking wine, soy sauce, meat broth, pepper powder, salt, fried tofu, winter mushrooms, and fresh peas, and boil for 10 minutes.

　　Secondly, for hepatitis D, it is advisable to consume

　　1. Ensure adequate caloric supply, with an appropriate daily intake of 8400 to 10500 kilojoules (2000 to 2500 calories).

　　2. Carbohydrates can generally account for 60 to 70% of total caloric intake.

　　3. To promote the repair and regeneration of liver cells, it is necessary to increase the supply of protein, which should generally account for 15% of total caloric intake. It is especially important to ensure a certain amount of high-quality protein, such as animal protein and soy products.

　　40. 4. Ensure the supply of vitamins. Vitamin B1, Vitamin B2, niacin, and other B-group vitamins as well as vitamin C play an important role in improving symptoms. In addition to choosing foods rich in these vitamins, multiple vitamin preparations can also be taken orally.

　　39. 5. Provide an adequate supply of liquids. Drinking more fruit juices, rice porridge, honey water, watermelon juice, etc., can accelerate the excretion of toxins and ensure the normal metabolic function of the liver.

　　38. 6. Prioritize high-quality protein foods such as fish, lean meat, eggs, milk, and soy products.

　　37. 7. Increase the intake of fresh vegetables and fruits.

　　36. Three. It is forbidden to eat for hepatitis D virus infection

　　35. 1. The high-calorie therapy for hepatitis that was once advocated is not advisable, as high calories can improve clinical symptoms, but can ultimately lead to fatty liver, which can worsen the condition, so the disadvantages outweigh the benefits.

　　34. 2. The high-sugar diet adopted in the past should also be corrected, as high-sugar diet, especially excessive glucose, fructose, and sucrose, can affect the appetite of patients, exacerbate gastrointestinal bloating, increase fat storage in the body, and lead to obesity and fatty liver. The supply of carbohydrates should mainly be through staple foods.

　　33. 3. Avoid fried and roasted foods and other strongly irritant foods, limit foods high in nitrogen extracts such as broths and chicken soups, to reduce the burden on the liver.

　　32. 4. Alcoholic beverages are strictly prohibited.

　　31. 5. Caution should be exercised with spicy and other irritant foods.

　　28. Treatment with a combination of traditional Chinese and Western medicine methods.
　　27. 1. When HBV and HCV are simultaneously infected, acute hepatitis is manifested, and the course of the disease is usually self-limiting, no special treatment is needed. The child should ensure rest, be given high-protein, high-vitamin, low-fat food, liver-protecting drugs, and traditional Chinese medicine treatment.
　　26. Treatment for chronic viral hepatitis caused by HBV and HDV superinfection:
　　25. (1) Antiviral Treatment: Interferon, once a day or three times a week, course of 3 to 6 months; Arabinosylcytosine injection in small doses, twice a day, course of 3 months.
　　24. (2) Immunomodulation: Thymosin injection or intravenous infusion twice or thrice a week, course of 1 to 2 months;
　　23. (3) Traditional Chinese Medicine Treatment.
　　22. If a child has symptoms of severe viral hepatitis, hospitalization for treatment should be immediate.