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Cloning, expression, and antiviral activity of interferon β from the Chinese microbat, Myotis davidii (Download the PDF)
# O& m; p/ }& U$ v W/ t/ A0 FYing-Zi Liang, Li-Jun Wu, Qian Zhang, Peng Zhou, Mei-Niang Wang, Xing-Lou Yang, Xing-Yi Ge, Lin-Fa Wang, Zheng-Li Shi*1 |3 ^% e M9 _" {: ~" o: q% H& T
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Abstract: Bats are natural reservoir hosts for many viruses that produce no clinical symptoms in bats.3 R0 }8 t6 S: j) b' V
Therefore, bats may have evolved effective mechanisms to control viral replication. However, little, E9 A! s% a l5 x% b( c( r
information is available on bat immune responses to viral infection. Type I interferon (IFN) plays a- O' r& n: ?2 |' F3 m; P4 s
key role in controlling viral infections. In this study, we report the cloning, expression, and
4 w! X5 X* } A9 }+ a: vbiological activity of interferon β (IFNβ) from the Chinese microbat species, Myotis davidii. We1 j2 K u9 x, i% F2 `
demonstrated the upregulation of IFNB and IFN-stimulated genes in a kidney cell line derived from* U2 l1 y. {' m
M. davidii after treatment with polyI:C or infection with Sendai virus. Furthermore, the recombinant
9 n% k; q: H) U6 D6 T2 @5 G: }/ ZIFNβ inhibited vesicular stomatitis virus and bat adenovirus replication in cell lines from two bat; ?$ h6 R" i0 e7 p+ E8 f; ]+ @
species, M. davidii and Rhinolophus sinicus. We provide the first in vitro evidence of IFNβ antiviral
4 l. {1 ~5 W; n N3 \/ w6 [8 E4 Dactivity in microbats, which has important implications for virus interactions with these hosts.
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/ m/ {5 R* X& u4 \) wKeywords: bat; interferon; IFN-stimulated genes; antiviral activity& |9 {$ T. j" U; Y& e* P
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中文信息:! A2 \+ I) Y, O _ L
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大卫鼠耳蝠干扰素β的克隆、表达和抗病毒活性检测
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梁英子,吴利军,张倩,周鹏,王媚娘,杨兴娄,葛行义,王林发,石正丽*; P3 [+ ]/ a8 E( z: u8 S
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摘要:蝙蝠是多种病毒的自然宿主,其中一些病毒是人畜新发传染病的病原。然而自然携带或人工感染病毒的蝙蝠并不表现出临床症状,其中机制未知。近期对两种蝙蝠基因组序列分析结果提示,蝙蝠可能具有一些独特的先天性免疫机制。本论文在前期研究基础上,用定量PCR技术分析病毒感染后蝙蝠干扰素及其诱导基因的应答水平;表达鼠耳蝠Ⅰ型干扰素和干扰素诱导蛋白,测试蝙蝠干扰素在不同来源的细胞中对病毒的抑制作用,试图初步了解病毒诱导的蝙蝠先天性免疫应答机制。" e$ r! ?; U" M2 E& l/ y
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7 m( `! ^% }7 h8 b) a关键词:干扰素,蝙蝠天然免疫,抗病毒活性,定量PCR4 ?+ y$ U0 p( O6 T! R& \3 o; R
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