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Developments In Hepatitis Delta Research

机译：肝炎三角洲研究的进展

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The hepatitis delta virus (HDV) is the smallest human pathogen known so far. Several characteristics of the virus RNA genome resemble that of plant viroids. Since the hepatitis B virus surface antigens are part of the HDV envelope and are necessary for productive infection, HDV may be considered a satellite virus of HBV. Coinfection of the two viruses or superinfection with HDV in HBV carriers increases the risk of fulminant hepatitis and development of liver cirrhosis. At present, there is no specific treatment for hepatitis D. However, vaccination against HBV confers protection against coinfection with HDV. Although the increased rate of vaccination against HBV in developed countries reduced the prevalence of HDV, it is still a threat and remains endemic in many regions of the world. Here, we overview the epidemiology and treatment of hepatitis delta and report recent advances in the research of HDV biology. Clinical and Epidemiological Features The hepatitis delta virus (HDV) was discovered by the italian gastroenterologist Mario Rizzetto while studying liver biopsies of hepatitis B virus (HBV) infected patients (Rizzetto et al., 1977). Later, it was shown that HDV infects individuals previously infected with HBV, causing more severe hepatic lesions, and increasing the risk of fulminat hepatitis (Gorinvadarajan et al., 1984; Jacobson et al., 1985). Since the presence of HBV is necessary for the production of infectious HDV particles capable of propagating the infection, the HDV may be considered a HBV satellite virus (Rizzetto et al., 1980; Ponzetto et al, 1988).The clinical association between these two viruses is due to the fact that the genome of HDV does not encode for its own envelope proteins. The HDV envelope consists of HBV surface proteins (HBsAg; Smedile et al., 1994), and as a consequence HDV transmission occurs only in the presence of HBV.HDV replication seems to occur only in the liver, and all pathological abnormalities are limited to this organ. The lesions are similar to those observed during the course of other acute and chronic viral hepatitis. Often they consist of hepatocellular necrosis and inflamation. From the histological point of view, there are no significant differences between lesions caused by HDV and those caused by other hepatitis viruses.The clinical course of HDV infection may be variable. In general, the observed symptoms are more severe than those associated with other hepatitis viruses. The incubation period varies between 3 to 7 weeks. Following this period, the first symptoms can be detected, including fatigue, lethargy, and nausea. It is estimated that 60% to 70% of all hepatitis delta chronic patients will develop chirrosis. This percentage is about three times higher when compared to the percentage that is observed in hepatitis B patients (Rizzetto et al., 1983). The frequency of HDV associated fulminant hepatitis, the more severe form of the acute disease, is 10 times higher than the observed for other viral hepatitis. Fulminant hepatitis is usually associated with hepatic encephalopaties that, in the most severe cases are characterized by somnolence, abnormal behavior, and coma. The mortality associated with fulminant hepatitis is about 80%, independent of the treatment (Purcell and Gerin, 1990).Seroprevalence studies in individuals positive for HBsAg, show a non-uniform worldwide distribution of HDV (Ponzetto et al., 1985; see fig. 1).
机译：肝炎三角洲病毒（HDV）是迄今为止已知的最小的人类病原体。病毒RNA基因组的几个特征类似于植物类病毒。由于乙型肝炎病毒表面抗原是HDV包膜的一部分，并且是生产性感染所必需的，因此HDV可以被视为HBV的卫星病毒。在HBV携带者中两种病毒的共同感染或HDV的双重感染增加了暴发性肝炎和肝硬化发展的风险。目前，尚无针对D型肝炎的具体治疗方法。但是，针对HBV的疫苗接种可预防HDV的合并感染。尽管发达国家对HBV的疫苗接种率提高了，但HDV的流行率仍然存在威胁，在世界许多地区仍然很流行。在这里，我们概述了肝炎三角洲的流行病学和治疗方法，并报告了HDV生物学研究的最新进展。临床和流行病学特征意大利胃肠病学家Mario Rizzetto在研究感染了乙型肝炎病毒（HBV）的患者的肝活检时发现了丙型肝炎三角洲病毒（HDV）（Rizzetto等，1977）。后来发现，HDV感染以前感染过HBV的个体，引起更严重的肝损伤，并增加了暴发性肝炎的风险（Gorinvadarajan等，1984; Jacobson等，1985）。由于HBV的存在对于产生能够传播感染的传染性HDV颗粒是必不可少的，因此可以将HDV视为HBV卫星病毒（Rizzetto等，1980; Ponzetto等，1988），两者之间的临床联系病毒是因为HDV的基因组不编码其自身的包膜蛋白。 HDV包膜由HBV表面蛋白组成（HBsAg; Smedile等，1994），因此HDV传播仅在HBV存在时发生，HDV复制似乎仅在肝脏中发生，并且所有病理异常仅限于这个器官。病变类似于在其他急性和慢性病毒性肝炎过程中观察到的病变。通常它们包括肝细胞坏死和炎症。从组织学角度看，HDV引起的病变与其他肝炎病毒引起的病变之间没有显着差异，HDV感染的临床过程可能会有所不同。通常，观察到的症状比与其他肝炎病毒相关的症状更严重。潜伏期为3至7周。在此期间之后，可以检测到最初的症状，包括疲劳，嗜睡和恶心。据估计，所有慢性乙型肝炎患者中有60％至70％会发展为手足病。与在乙型肝炎患者中观察到的百分比相比，该百分比大约高三倍（Rizzetto等，1983）。与HDV相关的暴发性肝炎（一种较严重的急性疾病）的发生频率是其他病毒性肝炎的10倍。暴发性肝炎通常与肝性脑病有关，在最严重的情况下，肝性脑病的特征是嗜睡，行为异常和昏迷。与暴发性肝炎相关的死亡率约为80％，与治疗无关（Purcell和Gerin，1990）.HBsAg阳性个体的血清阳性率研究表明，HDV在全球范围内分布不均匀（Ponzetto等人，1985年;见图） 1）。

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