庚型肝炎病毒感染对小儿慢性丙型肝炎的病理学影响

为观察庚型肝炎病毒（ＨＧＶ）感染对小儿慢性丙型肝炎（ＣＨＣ）的病理学影响，我们对近年来收治的１４岁以下的ＣＨＣ患者３１例血清标本进行了ＨＧＶＲＮＡ检测，并将合并与未合并ＨＧＶ感染者进行了病理学对比研究，现报道如下。对象：３１例患者以ＨＧＶＲＮ...     

庚型肝炎病毒感染状况研究

为了解小儿庚型肝炎病毒（ＨＧＶ）感染状况，对５０６例各型病毒性肝炎患儿，采用以ＨＧＶ合成肽为抗原的酶联免疫吸附技术（ＥＬＩＳＡ）检测抗ＨＧＶ。结果表明，ＨＧＶ在小儿组感染率为４．０％。小儿组甲、乙、丙型肝炎中ＨＧＶ感染率分别为１．５％、５．４％和１．６％。其中乙型肝炎中感染率高于其他型（Ｐ＜０．０５）。抗ＨＧＶ在急性肝炎的检出率为１．５％，慢性肝炎中为４．８％。提示ＨＧＶ感染在小儿肝炎中占有一定比例，并有其特点，应重视儿童ＨＧＶ感染的研究     

小儿感染庚型肝炎病毒后肝脏病毒核酸分布与临床关系的研究

目的 探讨小儿庚型肝炎病毒感染、肝脏庚型肝炎病毒核糖核酸（ＨＧＶ ＲＮＡ）分布与其他ＨＧＶ标志、肝脏病理损害及与临床的关系。方法 应用原位杂交（ＩＳＨ）检测１７例小儿乙型肝炎患儿肝脏ＨＧＶ ＲＮＡ。结果 １７例血清抗－ＨＧＶ阳性者,其中肝脏ＨＧＶ ＲＮＡ 阳性９例（９／１７,５３％）。肝脏ＨＧＶ ＲＮＡ 分布在汇周围,在肝小叶呈散在分布,多呈胞浆型;肝脏ＨＧＶ ＲＮＡ阳性组病变和阴性组比较以轻度（     

产前注射乙型肝炎免疫球蛋白预防乙型肝炎病毒宫内感染的临床研究

目的 减少新生儿宫内感染乙型肝炎病毒（ＨＢＶ）,探讨孕妇被动免疫预防ＨＢＶ宫内感染的作用。方法 将１４１例无症状ＨＢｓＡｇ（＋）孕妇随机分为两组,预防组６９例,自孕２８周起每月注射１次乙型肝炎免疫球蛋白（ＨＢＩＧ）,每次２００ ＩＵ;对照组７２例,不注射ＨＢＩＧ。在孕妇孕２８周、分娩前和新生儿出生时分别检测静脉血ＨＢｓＡｇ,ＨＢｅＡｇ和抗－ＨＢｓ,部分产妇检测乳汁ＨＢｓＡｇ,ＨＢｅＡｇ。结果 预防组新生儿血清ＨＢｓＡｇ检出率（５．８％）明显低于对照组（１６．７％）Ｐ＜０．０５;预防组新生儿抗－ＨＢｓ阳性率（３０．４％）显著高于对照组（９．７％）Ｐ＜０．０５;两组母亲乳汁ＨＢｓＡｇ检出率无显著差异。结论 产前多次肌注ＨＢＩＧ可减少携带ＨＢＶ母亲所生新生儿宫内受ＨＢＶ感染。     

表现为肾病综合征的乙型肝炎病毒相关性肾炎临床特点与诊断标准商榷

为总结本院４２例小儿乙型肝炎病毒相关肾炎（ＨＢＶ－ＧＮ）中表现为肾病综合征（ＢＶ＿ＮＳ）的临床特点,合并肝 受损情况并提出诊断标准意见。对４２例患儿活检的肾组织进行病理分型、免疫组化检测ＨＢＶ抗原及原位杂交法检测ＨＢＶＤＮＡ,结果：４２例占有６例血清ＨＢＶ感染标志阴性,其肾组织有５例病理类型为膜性肾炎及ＨＢＶ抗原阳性,６例ＨＢＶＤＮＡ均阳性,除外了继发性肾小球疾病,最终仍确诊为ＨＢＶ－ＮＳ。故认为     

应用原位杂交和原位聚合酶链反应技术检测肾组织中乙型肝炎病毒DNA

为深入探讨乙型肝炎病毒（ＨＢＶ）相关性肾炎的发病机理，应用地高辛素标记ＨＢＶＤＮＡ探针原位杂交和直接原位聚合酶链反应（ＰＣＲ）技术，对５例血清ＨＢＶ标志物阳性、临床诊断为ＨＢＶ相关性肾炎患儿的肾活检石蜡包埋组织切片行ＨＢＶＤＮＡ检测，并采用免疫组化ＬＳＡＢ法做标本的ＨＢＶ表面抗原（ＨＢｓＡｇ）检测。结果显示５例中有４例标本原位杂交和直接原位ＰＣＲ检测均呈ＨＢＶＤＮＡ阳性，ＨＢＶＤＮＡ阳性颗粒弥漫沉积于肾小球毛细血管袢、系膜区、肾小管及肾间质，表现形式以浆核型、核型为主；此４例ＨＢｓＡｇ亦阳性，ＨＢｓＡｇ阳性颗粒的分布与ＨＢＶＤＮＡ基本一致。提示ＨＢＶ不仅可通过免疫介导引起肾脏损害，而且有可能直接侵犯肾脏导致肾脏病变。     

阻断乙型肝炎病毒宫内传播的初步研究

宫内已感染乙型肝炎病毒（ＨＢＶ）是新生儿接种乙肝疫苗免疫失败的主要原因。为了减少新生儿产前在宫内受ＨＢＶ感染，提高乙肝疫苗接种后的免疫效果，研究给予阻断措施和观察其效果。从３６３２名孕妇筛查出ＨＢＶ无症状携带者２０４例，随机分为二组，即临产前３个月每月注射１次乙型肝炎免疫球蛋白（ＨＢＩＧ），每次２００ＩＵ，和不注射者作对照。在孕妇分娩后和新生儿出生时分别抽外周血作血清学检测。结果显示，ＨＢＩＧ组和对照组所生新生儿的宫内感染率分别是５．７％和１４．７％（Ｘ￣２＝４．５８，Ｐ＜０．０５）。分娩后二组孕妇的ＨＢｓＡｇ和ＨＢｅＡｇ的阳性率无差异，但ＨＢＩＧ组ＨＢｓＡｇ阳性滴度的均值显著低于对照组（ｔ＝４．８２，Ｐ＜０．０１）。提示产前多次肌注ＨＢＩＧ可减少携带ＨＢＶ母亲所生新生儿宫内受ＨＢＶ感染。这可能与产时减少母体外周血中的ＨＢＶ有关。接受ＨＢＩＧ在分娩前后的随访无不良反应。     

戊型肝炎病毒宫内感染及产儿死因研究

目的为了从分子水平探讨孕妇感染戊型肝炎病毒（ＨＥＶ）后胎儿宫内感染和死亡原因。方法对１７例患重症戊型肝炎的孕妇和娩出的１８例新生儿，以酶联免疫吸附法测母血和脐带血抗－ＨＥＶＩｇＭ／ＩｇＧ，同时查新生儿肝组织病理改变，免疫组化法查肝内戊型肝炎病毒抗原（ＨＥＶＡｇ），用地戈辛（ＤＩＧ）探针标记ＨＥＶｃＤＮＡ２３ｑｂｐ片段进行原位杂交查肝内ＨＥＶＲＮＡ。结果母血抗－ＨＥＶ、ＩｇＭ／ＩｇＧ均阳性，脐带血仅抗－ＨＥＶＩｇＧ阳性，肝组织以变性、炎变为主，新生儿肝内ＨＥＶＡｇ阳性率７７％（１０／１３），ＨＥＶ－ＲＮＡ阳性率６２％（８／１３）。结论ＨＥＶ存在宫内感染     

应用聚合酶反应技术检测婴儿肝炎综合征巨细胞病毒和乙型肝炎病…

用聚合酶以应技术（ＰＣＲ）检测６０例婴儿肝炎综合征患儿尿人巨细胞病毒（ＨＣＭＶ０ＤＮＡ在清乙型肝炎病毒（ＨＢＶ）ＤＮＡ，同时做尿ＨＣＭＶ病毒分离。结果表明：ＨＣＭＶ ＤＮＡ阳性４７例，阳性率７８．３％，而ＨＣＭＶ分离阳性３０例，阳性率５０．０％。ＨＢＶ ＤＮＡ阳性１２例，阳性一率２０％。提示婴儿肝炎综合征与ＨＣＭＶ和ＨＢＶ感染有关。ＰＣＲ技术特异，敏感，快速及简便，可协助临床医生对婴儿肝炎综合征做     

慢性乙型肝炎病毒携带者接种甲型肝炎疫苗

［英］／Ｎｅｂｂｉａ　Ｇ…／／ＪＰｅｄｉａｔｒ．－１９９９,１３６（６）．－７８４～７８５甲型肝炎（ＨＡ）预后通常良好,偶致暴发性肝功能衰竭．研究表明,慢性肝病者发生重度或暴发性ＨＡ的危险性增高．对３３例慢性乙型肝炎病毒感染患儿进行ＨＡ疫苗接种,以评价灭活ＨＡ疫苗的安全性及致免疫性．病人与方法３３例患儿中男２４例,女９例,中位年龄１０．７岁（２—１５岁）,血清抗ＨＡＶ均阴性,体健,均为慢性ＨＢｓＡｇ携带者,１８例ＨＢｅＡｇ阳性,１５例抗ＨＢｅ阳性,１３例血清丙氨酸氨基转移酶（ＡＬＴ）及天冬氨酸转…     

Hepatitis C and G Virus infections in polytransfused children

The prevalence of hepatitis C virus (HCV) and a newly identified hepatitis G virus (HGV) and their clinical significance were studied in 42 polytransfused Taiwanese children. Serological assays for antibodies against HCV (anti-HCV) and polymerase chain reaction for serum HCV ribonucleic acid (RNA) and HGV RNA were performed. The prevalence of anti-HCV and HGV RNA was 17% and 14%, respectively in 42 polytransfused children. Anti-HCV seropositives had a significantly higher mean age, peak serum transaminase level, and longer transfusion duration than seronegatives, while children with HGV infection usually had no or only mild hepatitis activities. The prevalence of anti-HCV dropped sharply after implementation of anti-HCV screening, however the prevalence of HGV viraemia remained unchanged. Conclusion HGV infection is not uncommon in polytransfused Taiwanese children and the virus does not cause significant hepatitis compared to HCV infection. Current blood donor screening for anti-HCV can effectively protect polytransfused children from HCV infection but the impact of additional screening for HGV markers awaits further studies. Received: 10 October 1996 and in revised form: 26 November 1996 / Accepted 26 November 1996     

Chronic viral hepatitis

Among hepatitis A to E viruses, hepatitis B, C, and D viruses can cause chronic hepatitis, in both children and adults. Hepatitis B virus (HBV) infection is the most prevalent and important one. Perinatal transmission accounts for about 40–45% of chronic HBV infection in hyperendemic areas. Horizontal transmission through intramuscular injection using non-sterile needles and intrafamilial spread accounts for the other half of carriers. During the natural course of HBV infection, the host gradually clears HBV and hepatitis B e antigen (HBeAg), liver damage and elevation of aminotransferases occur during the process of HBV clearance. The most effective way to eliminate HBV infection is immunoprophylaxis starting since birth. It can prevent both HBV and hepatitis D virus (HDV) infections. Hepatitis C virus (HCV) infection in children occurs mainly in high risk children, such as those who received blood product or injection using non-sterile needles, or infants of HCV viremic mothers, etc. Screening of blood product reduced markedly the prevalence of post-transfusion HCV infection, but the prevention of sporadic cases requires HCV vaccination which is still under investigation.     

Prevalence of hepatitis G virus in healthy children in liver disease, and human immunodeficiency virus-1 infection: response to interferon

BACKGROUND: A new virus of the Flaviviridae family, the hepatitis G virus (HGV/HGBV-C), has been identified recently. The purpose of this study was to determine the prevalence of HGV infection in healthy children, in patients with liver disease, and in human immunodeficiency virus (HIV)-1-infected patients. The role of HGV in the clinical course of chronic HCV, the response to interferon-alpha2b, and the possible implications of intravenous gamma-globulin in the transmission of the virus were also evaluated. METHODS: Fifty healthy children, 66 patients with a variety of liver diseases, 19 patients with acquired immune deficiency syndrome (AIDS), and various batches of commercial intravenous immunoglobulins were investigated. Viral HGV RNA (5'NCR-NS5) and anti-HGV envelope protein E2 were assayed. RESULTS: The prevalence of HGV infection was 6% in the healthy children and 42% in the liver disease group. Viremia and anti-E2 were found in 11% and 79% of patients with AIDS. Four (27%) of 15 patients with chronic HCV, receiving treatment with interferon, were coinfected by HGV and became HGV-RNA negative during therapy. One year after the end of interferon therapy, three of them were again HGV RNA positive. CONCLUSIONS: The prevalence of HGV infection is high in healthy children higher in children affected with liver disease, but its potential pathologic implication is questionable, and further studies are warranted. Hepatitis G virus is sensitive to interferon therapy, although the infection often recurs after discontinuation of treatment.     

GB virus C/hepatitis G virus infection in HIV infected patients with haemophilia despite treatment with virus inactivated clotting factor concentrates.

AIM: To determine the frequency of GB virus C (GBV-C)/hepatitis G virus (HGV) infection before and after switch to the use of virus inactivated concentrates in haemophiliac patients infected with human immunodeficiency virus (HIV). PATIENTS AND METHODS: Initial and follow up sera from 49 children with haemophilia were analysed for the presence of GBV-C/HGV RNA and antibodies to HGV (anti-HGV). All patients had been infected with HIV while receiving concentrates without virus inactivation before 1984 and were subsequently treated with virus inactivated concentrates. RESULTS: In the first available serum sample (1987 or later), two of 49 patients were GBV-C/HGV RNA positive and two further patients were anti-HGV positive. During follow up (mean, 6 years), 14 patients developed markers of GBV-C/HGV infection. Eleven of these had received no blood products except clotting factor concentrates that had been prepared with virus inactivation. CONCLUSIONS: Despite being treated with virus inactivated clotting factor concentrates, HIV positive patients with haemophilia are at an increased risk of manifesting GBV-C/HGV infection. We hypothesise that GBV-C/HGV is transmitted by these clotting factor concentrates. However, we cannot rule out the emergence of markers of GBV-C/HGV infection as a result of the progression of immune impairment in the course of HIV infection.     

High rate of maternal-infant transmission of hepatitis G virus in HIV-1 and hepatitis C virus-infected women

The prevalence of hepatitis G virus (HGV) infection was investigated in 56 mothers with both human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) infection. Thirty-three (58.8%) women had markers of HGV infection, including 7/15 (46.6%) with no history of parenteral exposure to blood. Sixteen (48%) had HGV RNA in serum by a polymerase chain reaction assay, and 17 (52%) had antibody to E2 viral protein. No woman was positive for both markers. Of 20 infants born to the 16 mothers with HGV viremia, 9 (45%, 95% CI 34-56%) acquired the infection. No infected child seroconverted to HGV during the first year of life. At the latest visit (mean: 37.1 mo, range: 9-89 mo) 7 children were still seronegative HGV RNA carriers, 1 was both RNA- and antibody-negative, while 1 RNA-negative child had developed the E2 antibody. Of the 20 HGV-exposed infants, 2 contracted HCV and 1 HIV-1 (all 3 with HGV coinfection). No abnormalities in clinical findings and ALT levels were observed throughout the follow-up period in the six children with HGV infection alone. Our findings show that HGV infection is widespread among HIV-1- and HCV-infected women. Maternal-infant transmission of HGV is common and occurs independently from that of HIV-1 and HCV in women with triple infection. Most perinatally HGV-infected children develop persistent infection with no clinical or biological signs of liver damage, at least in the first years of life.     

Transfusion-transmitted virus prevalence in Turkish patients with thalassemia

In hematology patients on chronic transfusion regimes, liver diseases are frequent, and mostly related to the agents transmitted by blood products and concominant iron deposition in liver. Besides hepatitis B (HBV) and C (HCV) viruses, new viral agents like hepatitis G virus (HGV) and TorqueTeno virus (TTV) are identified in these patients, although their association with any pathology or disease is not yet proved. In the present work, the authors studied the clinical importance of TTV in Turkish multitransfused patients with thalassemia. Forty-six healthy and 57 thalassemic patients were enrolled in the study. TTV was detected in serum samples by 3'-UTR nested PCR. Transaminase and ferritin levels, hepatitis B and C virus markers and number of transfusions were interpreted for possible association with TTV infection. As a result, TTV was detected in 63% of the thalassemia and 54% of the control patients. Prevalence of TTV infection, clinical features, laboratory data, and annual transfusion numbers of TTV-positive and -negative patients were not observed to be statistically significant. In conclusion, in Turkish patients with thalassemia, TTV infection cannot be considered as a risk factor for liver disease.     

广东地区婴肝患儿的HCV感染

目的探讨广东地区婴儿肝炎综合征中丙型肝炎病毒感染及其传播途径。方法采用酶联免疫吸附法（ELISA法）检测血清中丙型肝炎病毒（HCV）抗体，多聚酶链反应（PCR）检测血清中HCVRNA。结果90例婴肝中有11例HCV标志阳性，阳性率为12．2％（11／90），其中抗HCV以及HCVRNA均阳性4例，单项抗HCV阳性3例，单项HCVRNA阳性4例。母亲抗HCV阳性2例。结论HCV感染是广东地区婴儿肝炎综合征中一个不可忽视的病因，本组11例阳性患者的传播途径主要与输注血制品有关，其次为母婴传播。     

GB virus C/hepatitis G virus infection in HIV infected patients with haemophilia despite treatment with virus inactivated clotting factor concentrates

AIM—To determine the frequency of GB virus C (GBV-C)/hepatitis G virus (HGV) infection before and after switch to the use of virus inactivated concentrates in haemophiliac patients infected with human immunodeficiency virus (HIV).
PATIENTS AND METHODS—Initial and follow up sera from 49 children with haemophilia were analysed for the presence of GBV-C/HGV RNA and antibodies to HGV (anti-HGV). All patients had been infected with HIV while receiving concentrates without virus inactivation before 1984and were subsequently treated with virus inactivated concentrates.
RESULTS—In the first available serum sample (1987 or later), two of 49 patients were GBV-C/HGV RNA positive and two further patients were anti-HGV positive. During follow up (mean, 6 years), 14 patients developed markers of GBV-C/HGV infection. Eleven of these had received no blood products except clotting factor concentrates that had been prepared with virus inactivation.
CONCLUSIONS—Despite being treated with virus inactivated clotting factor concentrates, HIV positive patients with haemophilia are at an increased risk of manifesting GBV-C/HGV infection. We hypothesise that GBV-C/HGV is transmitted by these clotting factor concentrates. However, we cannot rule out the emergence of markers of GBV-C/HGV infection as a result of the progression of immune impairment in the course of HIV infection.

     

Serum zinc status in chronic hepatitis B and its relationship to liver histology and treatment results

BACKGROUND: It is known that cytotoxic T lymphocytes are responsible for viral clearance in chronic hepatitis B (HBV) infection. Zinc deficiency affects development of acquired immunity by preventing certain functions of T lymphocytes. We investigated the serum zinc levels and the relationship to liver histopathology and response to interferon alpha (IFN-alpha) and lamivudine combination therapy in 28 children with chronic HBV infection. METHODS: A course of IFN-alpha was injected as 5 million U/m2 subcutaneously, thrice a week for 6 months and lamivudine 4 mg/kg per day orally, for 1 year. Normalization of alanine aminotransferase (ALT), loss of HBV DNA, hepatitis B e antigen (HBeAg) seroconversion altogether was considered as end of therapy response (ETR). RESULTS: The ETR was achieved in eight (30.7%) patients. Serum zinc concentrations of 20 healthy children and patients was not significantly different (P>0.05). While pretreatment serum ALT, zinc, histological activity index (HAI) and portal inflammation scores were statistically higher in children who had ETR (P<0.005, P<0.05, P<0.05 and P<0.05, respectively), pretreatment serum HBV DNA was lower (P<0.005). Serum zinc level was correlated with HAI and portal inflammation scores (P<0.01 and P<0.01). CONCLUSION: This study showed the relationship of serum zinc status to liver histopathology and to the ETR and may be a preliminary study leading new studies focusing on zinc status in patients with chronic HBV infection.