从与近期暴发相关的一株病毒中拯救出野生型腮腺炎病毒有助于确定 SH ORF 在腮腺炎病毒发病机制中的作用。
Rescue of wild-type mumps virus from a strain associated with recent outbreaks helps to define the role of the SH ORF in the pathogenesis of mumps virus.
机构信息
Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, GA 30602, USA.
出版信息
Virology. 2011 Aug 15;417(1):126-36. doi: 10.1016/j.virol.2011.05.003. Epub 2011 Jun 14.
Mumps virus (MuV) causes acute infections in humans. In recent years, MuV has caused epidemics among highly vaccinated populations. The largest outbreak in the U.S. in the past 20 years occurred in 2005-2006 with over 5000 reported cases in which the majority of the cases was in vaccinated young adults. We sequenced the complete genome of a representative strain from the epidemic (MuV-IA). MuV-IA is a member of genotype G, the same genotype of MuV that was associated with the outbreak in the UK in 2004-2005. We constructed a reverse genetics system for MuV-IA (rMuV-IA), and rescued a virus lacking the open reading frame (ORF) of the SH gene (rMuV∆SH). rMuV∆SH infection in L929 cells induced increased NF-κB activation, TNF-α production and apoptosis compared to rMuV-IA. rMuV∆SH was attenuated in an animal model. These results indicated that the SH ORF of MuV plays a significant role in interfering with TNF-α signaling and viral pathogenesis during virus infection.
腮腺炎病毒（MuV）可引起人类急性感染。近年来，MuV 在高接种人群中引发了流行。美国过去 20 年中最大的一次疫情发生在 2005-2006 年，报告病例超过 5000 例，其中大多数病例发生在接种过疫苗的年轻成年人中。我们对疫情中具有代表性的一株（MuV-IA）进行了全基因组测序。MuV-IA 是基因型 G 的成员，与 2004-2005 年英国疫情中相关的 MuV 为同一基因型。我们构建了 MuV-IA 的反向遗传学系统（rMuV-IA），并拯救了一种缺失 SH 基因开放阅读框（ORF）的病毒（rMuV∆SH）。与 rMuV-IA 相比，rMuV∆SH 感染 L929 细胞可诱导 NF-κB 激活、TNF-α 产生和凋亡增加。rMuV∆SH 在动物模型中减毒。这些结果表明，MuV 的 SH ORF 在病毒感染过程中干扰 TNF-α 信号和病毒发病机制中起着重要作用。
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