January 2011 issue of the HBV Advocate’s Journal Review,

StephenW

http://www.hbvadvocate.org/news/HBJ8.1.htm

Selected extracts from the January 2011 issue of the HBV Advocate’s Journal Review, which showcases
the latest hepatitis B research into prevention, treatment, and infection transmission
从2011年1月的HBV倡导的杂志回顾，提取物，展示选定问题
最新的研究对于预防乙肝，治疗和传染

Tenofovir Effective  When Liver Failure Occurs and a Transplant Is Not Possible
Because of the shortage of available organs for liver  transplants, researchers have been searching for new methods to save patients  when they experience liver failure due to a spontaneous reactivation of their hepatitis  B.
Writing in the journal Hepatology,  researchers described using the antiviral tenofovir (Viread) in 14 HBV-infected  patients with high viral loads (HBV DNA) who experienced liver failure to see  if this treatment prolonged their lives.
After three months of treatment, 57% of those receiving  tenofovir survived, compared to only 15% of HBV-infected patients who did not  receive tenofovir, nor any other antiviral medication.
In the surviving patients, there was significant improvement  in liver health and a significant decline in the HBV-DNA levels.
Those who survived were found to experience a significant  reduction in HBV DNA after just two weeks of treatment.
泰诺福韦肝功能衰竭发生时有效和移植是不可能的由于可供移植的肝脏器官的短缺，研究人员一直在寻找新的方法来挽救病人肝功能衰竭的经验时，由于B型肝炎是他们自发活化
在期刊杂志写作，研究人员描述使用14 HBV感染高（乙肝病毒DNA）的肝衰竭谁遇到这种治疗是否延长他们的生命病毒载量患者的抗病毒泰诺福韦（VIREAD的）。
治疗3个月后，那些接受泰诺福韦57％存活，而只有15％的乙肝病毒感染者谁没有收到泰诺福韦，也没有任何其他抗病毒药物。
在幸存的患者，有显着改善肝脏健康，在HBV - DNA水平显着下降.
那些幸存下来，发现谁在乙型肝炎病毒DNA的经验后仅两个星期的治疗显着减少。

F141L Mutation in the  Surface Antigen Be Trigger That Causes Liver Cancer
Researchers continue to search for the mutation or viral  trigger that causes some people with hepatitis B to develop liver cancer. South  Korean researchers reported in the January 2011 issue of the Journal of  Virology that they may have found a mutation in the surface covering of the  virus, called HBsAg, that may play a role in causing liver cancer.
They identified a mutation called F141L and looked for that  in the surface antigen of 241 Korean patients with liver diseases at different  stages.
They found F141L mutants were present in a significant  number of liver cancer cases. The mutation was present in cancer cases more  often than was cirrhosis—severe liver scarring—which is often considered a  precursor to liver cancer.
“Our results suggest that (F141L) may contribute importantly  to the [development] of liver cancer by inducing cell proliferation and  transformation,” they wrote. They suggest that the F141L mutation could serve  as a diagnostic test for liver cancer.
F141L在表面抗原突变成为导致肝癌的触发
研究人员继续寻找突变或病毒引起，导致一些人与B型肝炎肝癌发展。韩国研究人员在2011年1月的病毒学杂志上，他们可能已经发现了病毒的覆盖面突变报道，被称为乙肝表面抗原，这可能在导致肝癌的作用。
他们发现了一个名为F141L突变，并期待在241肝病患者表面抗原韩国，在不同的阶段。
他们发现F141L突变体在肝癌症病例大量存在。突变是在目前的癌症病例往往比肝硬化重度肝脏上的疤痕，常常被认为是肝癌的前兆。
“我们的研究结果表明：（F141L）可能作出重要贡献，诱导细胞增殖和转化为肝癌[发展]，”他们写道。他们认为，F141L突变可作为肝癌诊断测试。

New, More Accurate Cause of  Fibrosis Identified
A multinational research team,  including scientists from the University of California, San Diego School of  Medicine, have for the first time accurately identified how fibrosis forms in  the liver, and how these fibrotic cells multiply and produce cirrhosis.
Their findings, published in the Proceedings  of the National Academy of Sciences, identify a previously unknown kind of  inflammatory white blood cell as the culprit behind liver fibrosis. Their  report completely changes current beliefs about how fibrosis develops in livers  infected by the hepatitis B virus (HBV).
When the liver is diseased,  healthy liver tissue is progressively replaced by fibrous scarring, which impairs  liver functioning. Ultimately, severe fibrosis results in cirrhosis and  contributes to liver cancer and failure, the 12th leading cause of death by  disease in the United States.
For years, scientists did not  understand how these fibroblast cells were created and assumed they were simply  transformed “epithelial” cells. Based on that assumption, they measured  fibroblast-specific protein 1 (FSP1) to determine if fibrosis was present in a  patient.
However, this new research shows  that FSP1 is not a reliable marker for fibrosis. Instead, endogenous stellate  cells appear to be the culprit in the development of fibrosis. However,  scientists did find that FSP1 was a consistent marker for a previously  unknown subset of inflammatory white blood cells or macrophages found in  injured livers.
新的，更准确的纤维化原因查明
一个多国研究小组，包括来自美国加州大学圣地亚哥分校医学院的科学家，有准确地确定如何在肝纤维化的形式，以及如何将这些细胞的繁殖并产生纤维化肝硬化的第一次。
他们的研究结果，在美国国家科学院学报上发表，标识为肝纤维化的罪魁祸首背后白血细胞炎症以前未知的种类。他们的报告完全改变有关如何纤维化由乙型肝炎病毒（HBV）感染肝脏的发展目前的观点。
当肝脏疾病，健康的肝脏组织，逐步取代纤维疤痕，这损害肝功能。最终，在肝硬化严重纤维化的结果，并有助于肝癌和失败，在12日由美国疾病死亡的首要原因。
多年来，科学家们不明白如何将这些成纤维细胞创造出来，以为他们在根本转变“上皮”细胞。在此假设的基础上，他们测量成纤维细胞特异性蛋白1（FSP1），以确定是否纤维化的病人中。
然而，这一新的研究表明，FSP1是不是纤维化的可靠指标。相反，内生星状细胞似乎是在肝纤维化发展的罪魁祸首。然而，科学家们发现，FSP1是一个白血细胞的炎症或损伤肝脏发现以前未知的巨噬细胞集一致的标记。

Neuromuscular Problems Common  Among Patients Taking Telbivudine
With increased, long-term use of  antivirals, researchers are increasingly identifying nerve and muscle damage as  side effects from this treatment. In a recent issue of the Journal of Viral  Hepatitis, researchers reported on their findings into neuromuscular and  nerve damage from the antiviral telbivudine (Tyzeka).
The scientists measured creatine  kinase (CK), an enzyme that is released into the blood when muscle tissue is  damaged, and they monitored patients for myopathy, a disease of the skeletal  muscles.
They measured CK levels in 200  patients treated with telbivudine for hepatitis B between January 2007 and July  2010. The 3-year cumulative incidence of CK elevations and myopathy was 84.3%  and 5%, respectively. CK elevations occurred more frequently in men than in  women, and in patients aged 45 and older who tested negative for the hepatitis  B “e” antigen (HBeAg-negative). Viral load did not appear to have an impact on CK  elevations.
CK elevations usually occurred 21  months after starting the antiviral, and most patients stopped having CK  elevations spontaneously without having to stop telbivudine treatment. However,  three patients had to switch to other antiviral agents.
“In conclusion, CK elevations are  common adverse reactions associated with telbivudine therapy, while myopathy is  rare,” researchers wrote.
神经肌肉患者服用替比夫定中存在的问题共同
随着增加，长期使用抗病毒药物，研究人员正在越来越多地查明神经和肌肉从这种治疗副作用的损害。在一本杂志上最近病毒性肝炎问题，研究人员报告了他们的发现为神经肌肉和神经的抗病毒药物替比夫定（Tyzeka）的伤害。
科学家测肌酸激酶（CK），一个是进入肌肉组织被破坏时，血液中释放酶，它们监测肌病，骨骼肌的疾病的患者。
他们测量与替比夫定治疗乙肝2007年1月至2010年7月200例对照的水平。 3年的CK升高和肌病的累积发生率分别为84.3％和5％，分别为。对照升高更频繁发生在男性多于女性，而在45岁以上患者谁检测乙型肝炎“e”的抗原（HBeAg阴性）阴性。病毒载量并未有一对CK升高的影响。
对照升高通常发生21个月启动后，抗病毒，大多数患者无需停止后停止替比夫定治疗的对照海拔自发的。然而，3例患者改用其他抗病毒药物。
“最后，对照升高与替比夫定治疗相关的常见不良反应，而肌病是罕见的，”研究人员写道。