Akabane virus nonstructural protein NSm regulates viral growth andpathogenicity in a mouse model

Journal of Veterinary Medical Science

Keita SUGIURA³  Akiko TAKENAKA-UEMA³  Kohei SAEKI²  Tatsuya IWANAGA³  Norasuthi BANGPHOOMI³  Kentaro KATO³  Chieko SHIODA¹  Shin MURAKAMI³  Yukari ISHIHARA³  Shumpei TSUDA³  Kazuyuki UCHIDA¹  Taisuke HORIMOTO³  Hiroomi AKASHI³ 

[1] Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1�?1�?1 Yayoi, Bunkyo-ku, Tokyo 113�?8657, Japan;Department of Veterinary Surgery, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1�?1�?1 Yayoi, Bunkyo-ku, Tokyo 113�?8657, Japan;Department of Veterinary Microbiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1�?1�?1 Yayoi, Bunkyo-ku, Tokyo 113�?8657, Japan

关键词: Akabane virus;    nonstructural protein;    pathogenicity;    reverse genetics;   

DOI  :  10.1292/jvms.16-0140

学科分类：兽医学

来源: Japanese Society of Veterinary Science

【 摘 要 】

References(16)The biological function of a nonstructural protein, NSm, of Akabane virus (AKAV) isunknown. In this study, we generated a series of NSm deletion mutant viruses by reversegenetics and compared their phenotypes. The mutant in which the NSm coding region wasalmost completely deleted could not be rescued, suggesting that NSm plays a role in virusreplication. We next generated mutant viruses possessing various partial deletions in NSmand identified several regions critical for virus infectivity. All rescued mutant virusesproduced smaller plaques and grew inefficiently in cell culture, compared to the wild-typevirus. Interestingly, although the pathogenicity of NSm deletion mutant viruses varied inmice depending on their deletion regions and sizes, more than half the mice died followinginfection with any mutant virus and the dead mice exhibited encephalitis as in wild-typevirus-inoculated mice, indicating their neuroinvasiveness. Abundant viral antigens weredetected in the brain tissues of dead mice, whereas appreciable antigen was not observedin those of surviving mice, suggesting a correlation between virus growth rate in thebrain and neuropathogenicity in mice. We conclude that NSm affects AKAV replicationin vitro as well as in vivo and that it may functionas a virulence factor.

【 授权许可】

Unknown