营养状况会影响乙肝病毒 - 学术讨论& HBV English

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发表于 2006-10-19 21:24 |只看该作者 |倒序浏览 |打印

营养状况会影响乙肝病毒

（因为我对代谢以及乙肝病毒都很有兴趣，今天读到这篇文章觉得非常不错。）

2006年10月16日在美国科学院院报发表。以色列研究人员的工作。

标题

GC-1A 根据营养状况控制乙肝病毒。

大意：作者发现短期禁食会诱导乙肝病毒基因表达，这种诱导是通过PGC-1A 依赖性的。可以通过重新进食抑制乙肝病毒基因表达。

意义：
乙肝病毒为什么喜欢肝脏？这个问题也许能找到对付乙肝病毒的方法。
保持稳定的身体状况，生活有规律可能会与乙肝病毒和平相处。
如果体内状况有变化，比如禁食或其他剧烈变化情况，就有可能刺激乙肝病毒的变得活跃。
这也许可能解释为什么过度疲劳会诱发肝病。

这篇文章清楚地说明乙肝病毒与身体代谢状况联系的一个关键分子 PGC-1A。
也许能对战胜乙肝病毒开启一条全新的思路。

1: Proc Natl Acad Sci U S A. 2006 Oct 16; [Epub ahead of print]Click here to read Links
    PGC-1{alpha} controls hepatitis B virus through nutritional signals.

        * Shlomai A,
        * Paran N,
        * Shaul Y.

    Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot 76100, Israel.

    Hepatitis B virus (HBV) is a 3.2-kb DNA virus that replicates preferentially in the liver. Liver-enriched nuclear receptors (NRs) play a major role in the HBV life cycle, operating as essential transcription factors for viral gene expression. Notably, these NRs are also key players in metabolic processes that occur in the liver, serving as central transcription factors for key enzymes of gluconeogenesis, fatty acid beta-oxidation, and ketogenesis. However, the association between these metabolic events and HBV gene expression is poorly understood. Here we show that peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha), a major metabolic regulator and a coactivator of key gluconeogenic genes, robustly coactivates HBV transcription. We further demonstrate that the liver-enriched NR hepatocyte nuclear factor 4alpha that binds HBV plays an important role in this process. Physiologically, we show that a short-term fast that turns on the gluconeogenic program robustly induces HBV gene expression in vivo. This induction is completely reversible by refeeding and depends on PGC-1alpha. We conclude that HBV is tightly regulated by changes in the body's nutritional state through the metabolic regulator PGC-1alpha. Our data provide evidence for nutrition signaling to control viral gene expression and life cycle and thus ascribe to metabolism an important role in virus-host interaction.

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