乙型肝炎患者血清中HBVDNA含量与HBV血清学标志关系

[目的 ]　探讨乙型肝炎患者血清中HBVDNA含量与HBV血清学标志的关系。 [方法 ]　测定不同乙肝血清学标志模式和 2 47份标志物全阴性的临床肝炎病人血清以半套式PCR荧光定量检测系统检测HBVDNA含量。 [结果 ]　在HBsAg、HBeAg阳性的血清中HBVDNA含量最高 ,血清HBeAg和HBVDNA含量密切相关。但在很少数HBeAg阳性血清中未能检出HBVDNA。在另外的乙肝血清标志物模式中 ,包括全阴性和抗HBs阳性 ,也有少数血清标本能检出HBVDNA ,其浓度分布的范围很广。 [结论 ]　少数血清HBsAg、HBeAg阳性的病人并不处于HBV活跃复制的状态。PCR定量检测HBVDNA含量更有助于乙肝的预后和抗病毒疗效的监测。     

乙型肝炎患者血清HBV-DNA与HBeAg的关系

[目的 ]探讨乙型肝炎患者血液中HBV病毒含量与血清HBeAg之间的关系。[方法 ]用荧光定量聚合酶链反应(FQ PCR)检测乙肝病人血清中的HBV DNA含量 ,用ELISA法检测血清中乙肝标志物e抗原 (HBeAg)。[结果 ]HBeAg阳性组其HBV DNA检出率 10 0 %,且含量明显高于HBeAg阴性组 (P <0 0 1) ,HBeAg阴性组中HBV DNA阳性检出率为49 7%。检验结果能有效反应乙肝的临床治疗和监测发现。 [结论 ]用FQ PCR能直接 ,准确地反映乙肝患者体内病毒复制水平。对乙肝诊断、指导临床用药和治疗监测方面具有实用价值。     

慢性乙肝HBV DNA定量与e系统及ALT检测结果

乙型肝炎病毒 (HBV)感染的诊断及疗效主要依据血清学标志物和HBV DNA等的检测 ,其中HBV DNA是HBV感染、复制和传染性强弱的直接指标[1 ] 。我们用荧光定量PCR法检测 2 13例慢性乙肝患者血清HBV DNA含量 ,同时用ELISA法检测HBV标志物及ALT水平 ,分析HBV -DNA含量与HBV血清学标志物及肝功能的关系。对象与方法1　对象　慢性乙肝病人血清标本 199例 ,根据HBeAg与抗HBe分组 ,HBeAg (+)、抗HBe (- ) 94例为A组 ,HBeAg (- )、抗HBe (+) 10 5例为B组。2　方法　 (1)HBVDNA的检测 :荧光定量PCR法检测HBV -DNA ,试剂…     

乙肝病毒前S2抗原的临床应用

目的探讨乙型肝炎病毒前S2抗原(Pre-S2)检测在临床中的应用价值。方法将253例乙型肝炎患者标本用酶联法(ELISA)检测Pre-S2、乙型肝炎病毒(HBV)标记物,荧光定量PCR法检测乙型肝炎病毒DNA(HBVD-NA)。结果HBeAg阳性组Pre-S2、HBVDNA阳性率各为95.3%、97.6%;抗-HBe阳性组Pre-S2、HBVDNA阳性率各为58.1%、31.2%;e系统阴性组Pre-S2、HBVDNA阳性率各为74.7%、45.3%。结论乙型肝炎患者Pre-S2与HBeAg、HBVDNA呈伴随关系,是HBV复制活跃和疗效观察的良好指标;抗-HBe阳性及e系统阴性乙型肝炎患者Pre-S2检出率偏高有待探讨。     

HBsAg和HBcAg在慢性乙肝病毒携带者肝组织中的表达

目的观察慢性乙肝病毒携带者血清标志物与肝组织HBcAg表达的相关性。方法对80例慢性乙肝病毒携带者行快速经皮肝穿刺术取肝组织，免疫组化染色检查HBsAg，HBcAg。荧光定量PCR法检测血清HBVDNA。ELISA法检测血清HBsAg、抗-HBs、HBeAg、抗-HBe和抗-HBc。结果血清HBsAg均阳性，血清HBeAg阳性者48例、HBeAg阴性者32例，血清HBVDNA阳性者50例、HBVDNA阴性者30例。肝组织HBsAg阳性者68例、肝组织HBcAg阳性者43例。结论慢性乙肝病毒携带者肝组织HBcAg表达与血清标志物HBVDNA、HBeAg有相关性。     

实时荧光定量聚合酶链反应检测唾液HBV-DNA含量

目的:采用实时荧光定量聚合酶链反应(FQ-PCR)方法准确地定量检测血清、唾液中乙型肝炎病毒(HBV)的数量和免疫指标,进而全面评估唾液乙肝DNA在乙型肝炎的预防、诊断及治疗方面的意义。方法:采用FQ-PCR法检测200例乙型肝炎患者血清、唾液中HBVDNA的含量。结果:(1)经FQ-PCR检测,200份标本中血清HBVDNA含量>103copies/ml的有180例(90%),相应的唾液中HBVDNA含量>103copies/ml的有145例(72.5%),同时病毒含量>105copies/ml标本中血清168例(84.0%),唾液98例(49.0%),血清HBVDNA与唾液HBVDNA水平之间存在显著相关(r=0.79,P<0.001)。(2)在不同的血清免疫指标组合中乙肝病毒含量也不相同,在HBeAg( )组与HBeAg(-)组中,血清与唾液的病毒含量与阳性率均存在HBeAg( )组明显高于HBeAg(-)组,在HBeAg( )组中血清、唾液HBVDNA平均水平分别为7.13、5.01 logcopies/ml。血清、唾液病毒含量在两组不同免疫组合中差别均有统计学意义(P<0.01)。结论:(1)乙型肝炎患者除了血清外,唾液中也存在具有感染性的高病毒载量HBVDNA,可能成为传染源之一。(2)唾液中定量检测HBVDNA与血液中HBVDNA含量存在明显相关性,在一定程度上也能反映HBVDNA在体内复制情况。     

慢性乙型肝炎患者定量检测HBV BNA及其临床意义

目的 比较慢性乙型肝炎患者血清中HBeAg阳性和阴性与HBV DNA含量之间的关系并分析其临床意义.方法 采用微粒子发光分析法检测102例患者血清中HBeAg含量,同时采用荧光定量PCR法检测患者血中HBV DNA含量,并进行比较分析.结果 HBeAg(+)血清54例,HBV DNA平均含量为(7.53±1.08)E copies/ml;HBeAg(-)血清48例,HBV DNA平均含量为(5.13±1.33)E copies/ml,两组具有显著差异(P＜0.001).102例患者血清HBeAg和HBV DNA含量与ALT(丙氨酸氨基转移酶)无相关关系.结论 血清中HBeAg阳性和阴性与HBV DNA含量有一定相关性,与ALT无相关关系,临床应结合两者对病情进行综合判断.     

慢性乙型肝炎患者定量检测HBV DNA及其临床意义

目的比较慢性乙型肝炎患者血清中HBeAg阳性和阴性与HBV DNA含量之间的关系并分析其临床意义。方法采用微粒子发光分析法检测102例患者血清中HBeAg含量,同时采用荧光定量PCR法检测患者血中HBV DNA含量,并进行比较分析。结果HBeAg( )血清54例,HBV DNA平均含量为(7.53±1.08)E copies/ml;HBeAg(-)血清48例,HBV DNA平均含量为(5.13±1.33)E copies/ml,两组具有显著差异(P<0.001)。102例患者血清HBeAg和HBV DNA含量与ALT(丙氨酸氨基转移酶)无相关关系。结论血清中HBeAg阳性和阴性与HBV DNA含量有一定相关性,与ALT无相关关系,临床应结合两者对病情进行综合判断。     

血清中前S1抗原与HBV-DNA、HBeAg检测结果及临床意义的分析

目的对比分析前S1抗原、HBV—DNA和HBeAg在乙型肝炎感染期主要临床意义。方法用酶联免疫吸附法（ELISA）分别检测前S1抗原和乙肝血清标志物“五项”，用荧光定量聚合酶反应（PCR）检测HBV—DNA，对619例乙肝病毒标志物进行检测，检测结果进行统计分析。结果619例中HBV-DNA阳性率78．4％[485／619]，前S1抗原的阳性率为69．34％[429／619]，其中HBeAg阳性／HBeAg阴性[HBeAb阳性]又分为两组，结果：前S1抗原阳性率在EBeAg阳性模式组中明显高于HBeAg阴性／抗HBeAb阳性模式组，前S1抗原与HBV—DNA和HBeAg检测有明显相关性和互补性。结论前S1抗原的检测可以较好的反映HBV存在和复制的情况，前S1抗原作为辅助或补充指标联合HBV血清标志物与HBV—DNA同步动态监测，为乙型肝炎的诊断、治疗和预后判断提供依据，具有重要临床价值。     

1517例乙肝标志物和HBV-DNA定量相关性分析

目的探讨血清HBV-DNA水平与HBV血清标志物的相关性。方法采用实时荧光定量PCR对1517例HBV感染者血清标本中HBV-DNA含量进行检测,同时用ELISA法检测其HBV免疫标志物。结果HBsAg、HBeAg、HBcAb阳性组患者血清HBV-DNA检出率98.24%;HBsAg、HBeAg阳性组为100.00%;HBsAg、HBeAb、HBcAb阳性组为60.98%;HBsAg、HBcAb阳性组为37.71%;HBcAb阳性组为12.90%。结论患者血清HBV-DNA的阳性率与HBV血清标志物的存在状态相关,采用FQ PCR法检测HBV-DNA能更准确、直接地反映体内病毒复制情况。     

Control of bovine virus diarrhoea virus

Bovine virus diarrhoea (BVD) virus is ubiquitous in cattle populations throughout the world. Strategies for controlling BVD virus infections are continually evolving. Current control procedures are based on identification and elimination of persistently infected cattle, which are a primary source of virus for non-infected cattle, and immunisation with killed or modified live virus vaccines. Additional concerns for control are the possible contamination of semen, embryos and biologicals with virus. In the near future, genetically engineered nucleic acid probes and subunit vaccines containing selected elements of the BVD virus may be available for incorporation into control procedures.     

Epidemiology of bovine virus diarrhoea virus

A better understanding of the epidemiology and pathogenesis of bovine virus diarrhoea virus (BVDV) has emerged in recent years. Fetal infections and in particular those resulting in birth of persistently infected calves are of central importance for the epidemiology of BVDV. A prevalence of persistently infected, viraemic animals of about 1% is found in Denmark and elsewhere by examination of randomly collected blood samples. A recent field study shows that 53% of randomly selected herds in an area in Denmark where BVDV is endemic had one or more persistently infected animals. Persistently infected cows may breed and will always transmit the infection to the calf. Such familial occurrence of persistent infection seems to be a fairly common phenomenon. Persistently infected cattle are important sources of infection to other cattle. Transiently infected cattle following experimental exposure will usually not transmit the infection by contact but this may not always apply to cattle after natural infection. Knowledge of the occurrence and potential for spread of virus from persistently infected bulls is reviewed. Virus is excreted with semen of both persistently and transiently infected bulls and BVDV may be transmitted by use of infected semen for insemination. The potential for spread of the infection through embryo transfer should be avoided by the use of adequate testing and controls.     

Bovine virus diarrhoea virus: an introduction

In view of the recently established genome organisation of pestiviruses, their classification as members of the togavirus family is no longer tenable. They should rather be provisionally considered as a new genus of the Flaviviridae, irrespective of differences in the nonstructural genes. Like other positive-stranded RNA viruses, pestiviruses are highly variable; apart from point mutations, recombinations are expected to contribute to their capricious behaviour. One trait of expected pathogenetic significance in infections with bovine virus diarrhoea virus is a change from the non-cytopathogenic to a cytopathogenic biotype. Cooperation of both variants in an animal to produce the severe disease picture known as mucosal disease is unique in virology; elucidation of this mechanism may shed light on the pathogenesis of other sporadic diseases with suspected viral origin.     

Electron microscopy of bovine virus diarrhoea virus

Bovine virus diarrhoea virus (BVDV) has been (tentatively) identified by electron microscopy in purified virus preparations, in infected cell cultures and in tissues and cells from infected animals. These studies have revealed a spherical membrane-bound particle with a diameter of 40-60 nm. The membrane is smooth, bilaminar and surrounds a dense or semi-dense core of 20-25 nm. The core particle may be isometric or hexagonal. In studies of the morphogenesis of BVDV in infected cell cultures, it was found that assembly and maturation of the viral particles occur via a condensation process within membrane-bound vesicular organelles, in which the virions subsequently accumulate. Release of the virus occurs when the cell finally lyses and/or via exocytosis. Thus, both with regard to morphogenesis and to morphology, BVDV bears close resemblance to the Flaviviridae.     

Molecular biology of bovine virus diarrhoea virus

Our understanding of the molecular biology of bovine virus diarrhoea virus (BVDV) has greatly increased over the past several years. The development of monoclonal antibodies (MAB's) has identified a key antigen of BVDV while at the same time providing evidence for considerable variation in this protein. MAB's, particularly those directed against the p80 protein, can be developed for use in diagnostic tests while others may be useful in molecular epidemiological studies of BVDV. The successful cloning of BVDV and hog cholera virus can provide nucleic acid probes for use in routine diagnostic testing, for use in pathogenesis studies and for the detection of BVDV contamination in biological materials. With the identification of the key antigens of BVDV and its molecular cloning, the future holds the promise of vectored vaccines which can provide the efficacy of modified-live vaccines with the safety of killed vaccines. However, much work still must be done to define the significance of the antigenic variation of BVDV as it relates to providing protection for the developing fetus.     

Hendra virus and Nipah virus animal vaccines

Hendra virus (HeV) and Nipah virus (NiV) are zoonotic viruses that emerged in the mid to late 1990s causing disease outbreaks in livestock and people. HeV appeared in Queensland, Australia in 1994 causing a severe respiratory disease in horses along with a human case fatality. NiV emerged a few years later in Malaysia and Singapore in 1998–1999 causing a large outbreak of encephalitis with high mortality in people and also respiratory disease in pigs which served as amplifying hosts. The key pathological elements of HeV and NiV infection in several species of mammals, and also in people, are a severe systemic and often fatal neurologic and/or respiratory disease. In people, both HeV and NiV are also capable of causing relapsed encephalitis following recovery from an acute infection. The known reservoir hosts of HeV and NiV are several species of pteropid fruit bats. Spillovers of HeV into horses continue to occur in Australia and NiV has caused outbreaks in people in Bangladesh and India nearly annually since 2001, making HeV and NiV important transboundary biological threats. NiV in particular possesses several features that underscore its potential as a pandemic threat, including its ability to infect humans directly from natural reservoirs or indirectly from other susceptible animals, along with a capacity of limited human-to-human transmission. Several HeV and NiV animal challenge models have been developed which have facilitated an understanding of pathogenesis and allowed for the successful development of both active and passive immunization countermeasures.     

Clinical aspects of bovine virus diarrhoea virus infection

Bovine virus diarrhoea virus (BVDV) infection of cattle results in a wide range of clinical manifestations. This article reviews the clinical responses associated with BVDV and discusses these diseases in terms of acute infection in immunocompetent cattle, fetal infection, infection in cattle immunotolerant to and persistently infected with BVDV and finally mucosal disease.     

The pathogenesis of bovine virus diarrhoea virus infections

Bovine virus diarrhoea virus (BVDV) disease in cattle ranges from the transient acute infections, which may be inapparent or mild, to mucosal disease which is inevitably fatal. On occasions the acute infections can lead to clinical episodes of diarrhoea and agalactia but as these syndromes cannot be reproduced experimentally, the pathogenesis remains unclear. The immunosuppressive effect of acute BVDV infections can enhance the clinical disease of other pathogens and this may be an important part of the calf respiratory disease complex. Although BVDV antigen has been demonstrated within the lymphoid tissues, for prolonged periods, the evidence for viral latency remains to be proven. Venereal infection is shown to be important in the transfer of virus to the foetus and congenital infections can cause abortions, malformations and the development of persistently viraemic calves. The two biotypes of the virus, non-cytopathogenic and cytopathogenic, are described. Their sequential role in the pathogenesis of mucosal disease arises from the initial foetal infection with the non-cytopathogenic virus and the subsequent production of persistently viraemic calves. These calves may later develop mucosal disease as a result of superinfection with a "homologous" cytopathogenic virus. The possible origin of this biotype by mutation is discussed. Chronic disease is defined as a progressive wasting and usually diarrhoeic condition; it is suggested that this may develop following superinfection of persistently viraemic cattle with a "heterologous" cytopathogenic biotype.     

Immunological responses to bovine virus diarrhoea virus infections

Infection of normal calves with bovine virus diarrhoea virus (BVDV) is a transient self-limiting infection that can result in a period of immunosuppression. The virus appears to be able to replicate in all of the major lymphocyte sub-populations as well as in accessory cells. This may result in the leukopenia that is often a sequel of infection and affects B-cells as well as the T-cell sub-populations expressing either BoCD4 or BoCD8 antigens. B and T-cell responses are affected as a consequence of exposure to BVDV and there is a reduced ability to control other infections. Evidence is summarised and shows that immunoglobulin is an important mediator of immunity to infection with BVDV. Although the foetus can mount an immune response in the latter part of gestation, during the first trimester it does not. A specific state of tolerance is induced and this is associated with change in the proportion of certain lymphocyte sub-populations and ability to respond to immune stimulation.