Melo-Silva Carolina R, Tscharke David C, Lobigs Mario, Koskinen Aulikki, Müllbacher Arno, Regner Matthias
Department of Emerging Pathogens and Vaccines, The John Curtin School of Medical Research, Australian National University, Canberra ACT, Australia.
Department of Immunology and Infectious Disease, The John Curtin School of Medical Research, Australian National University, Canberra ACT, Australia.
Virus Res. 2017 Jan 15;228:61-65. doi: 10.1016/j.virusres.2016.11.017. Epub 2016 Nov 16.
Mousepox is caused by the orthopoxvirus ectromelia virus (ECTV), and is thought to be transmitted via skin abrasions. We studied the ECTV virulence factor N1 following subcutaneous infection of mousepox-susceptible BALB/c mice. In this model, ECTV lacking N1L gene was attenuated more than 1000-fold compared with wild-type virus and replication was profoundly reduced as early as four days after infection. However, in contrast to data from an intranasal model, N1 protein was not required for virus dissemination. Further, neither T cell nor cytokine responses were enhanced in the absence of N1. Together with the early timing of reduced virus titres, this suggests that in a cutaneous model, N1 exerts its function at the level of infected cells or in the inhibition of the very earliest effectors of innate immunity.
鼠痘由正痘病毒埃可病毒（ECTV）引起，被认为通过皮肤擦伤传播。我们在对鼠痘易感的BALB/c小鼠进行皮下感染后，研究了ECTV毒力因子N1。在该模型中，与野生型病毒相比，缺乏N1L基因的ECTV减毒超过1000倍，并且早在感染后四天复制就大幅减少。然而，与鼻内模型的数据相反，病毒传播不需要N1蛋白。此外，在没有N1的情况下，T细胞反应和细胞因子反应均未增强。连同病毒滴度降低的早期时间，这表明在皮肤模型中，N1在受感染细胞水平或在抑制先天免疫的最早效应器方面发挥其功能。
