The comparison of virus genome and immune reaction between asymptomatic carriers and chronic hepatitis patients infected with HBV.

无症状携带者与乙型肝炎病毒感染者的病毒基因组及免疫反应比较

• 批准号: 13670495
• 负责人: MARUYAMA Toshiyuki
• 金额: $ 0.64万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2001
• 资助国家: 日本
• 起止时间: 2001 至 2002
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13670495/
• 关键词: HBV-DNA; tolerance; transgenic mouse; mutation; cytokine; HBV; 免疫応答; トランスジェニックマウス; 抗原提示; 核酸変異

Antigen presenting cells were induced from spleen cells of HBcAg transgenic mouse (Tg10c), or HBeAg transgenic mouse (Tg30e), and HBcAg transgenic mouse has the better ability to induce HBcAg specific antigen presenting activity, but lower ability to express HBeAg.Antibody production against HBcAg or or HbeAg was slightly low in Tg10c, and almost lost in Tg30e.20 asymptomatic HBV carrier patients (group A) who has no symptom and no elevation of liver function test and 25 HBV related chronic hepatitis patients (group B) were analyzed for virolo9ical profile and cYtokine production.Although few mutations were detected in group A patients, several mutations were found in group B patients. Lots of mutations were concentrated in the core region. However, chronic hepatitis B does not appear to be caused by a specific genomic mutation or an amino acid mutation.In the cytokine production assay, the average interleukin 2 levels were higher in group B patients than that in group A patients. Similarly, and IFNγ levels were higher in group B patients than that in group A patients.

从HBcAg转基因小鼠（Tg10c）和HBeAg转基因小鼠（Tg30e）脾细胞中诱导出抗原提呈细胞，HBcAg转基因小鼠具有较强的抗原提呈活性，但表达HBeAg的能力较弱，Tg10c小鼠产生抗HBcAg或HBeAg抗体的能力较低，20例无症状、肝功能无升高的无症状HBV携带者（A组）和25例HBV相关慢性肝炎患者（B组）A组患者中检测到少量突变，而B组患者中检测到多个突变。大量的突变集中在核心区域。然而，慢性B型肝炎似乎不是由特定的基因组突变或氨基酸突变引起的。在细胞因子产生测定中，B组患者的平均白细胞介素2水平高于A组患者。B组IFNγ水平高于A组。

项目成果

Moriya K., Koike K.: "Increase in the concentration of carbon 18monounsaturated fatty acids in the liver with hepatitis C : analysis intransgenic mice and humans."Biochemical & Biophysical Research Communications. 281. 1207-1212 (2001)

Moriya K.、Koike K.：“丙型肝炎导致肝脏中碳 18 单不饱和脂肪酸的浓度增加：转基因小鼠和人类的分析。”生物化学

Hirayama M., Maruyama T.: "IgG1 anti-P2 as a marker of response to interferon in patients with chronic hepatitis C."Clinical Experimental Immunology.. 126. 92-100 (2001)

Hirayama M.、Maruyama T.：“IgG1 抗 P2 作为慢性丙型肝炎患者干扰素反应的标志物。”临床实验免疫学.. 126. 92-100 (2001)

Moriya K.: "Oxidative stress in the absence of inflammation in a mouse model for hepatitis C virus-associated hepatocarcinogenesis."Cancer Research. 61. 4365-4370 (2001)

Moriya K.：“丙型肝炎病毒相关肝癌发生的小鼠模型中无炎症情况下的氧化应激。”癌症研究。

Maekawa H, Maruyama T, et al.: "Esophageal smooth muscle tumor in a 25 year old female with congenital malformations"J. of Gastroenterology. 36. 700-703 (2001)

Maekawa H, Maruyama T, et al.：“一名 25 岁先天性畸形女性食管平滑肌肿瘤”J.

Maruyama T.: "Response to precore stop mutant in anti-HBe positive phases of chronic hepatitis B virus infection"American Journal of Gastroenterology. 97. 2139-2140 (2002)

Maruyama T.：“慢性乙型肝炎病毒感染的抗 HBe 阳性阶段对 precore 停止突变体的反应”美国胃肠病学杂志。