GENETIC STUDIES OF ROTAVIRUS PATHOGENESIS

人们一直在努力描述遗传机制 轮状病毒在新生生猪模型中的潜在毒力。 一种单基因替换重组子，具有1，2，5，6， 来自人类轮状病毒DS-1株的第7、8或11个基因(它不 导致产后感染或腹泻)，以及 来自猪轮状病毒SB-1a株的剩余10个基因(它一直 引起仔猪腹泻)引起仔猪腹泻 与病毒脱落有关。然而，挑战小猪的是一只 具有VP3基因或VP4基因或VP7的基因替换重组体 DS-1病毒的NS-28基因和猪的其余10个基因 SB-1A型病毒未发病或脱毒。因此，我们演示了 第3、4、9(VP7)或第10(NS28)基因各自扮演着重要的角色 轮状病毒感染在仔猪致病中的作用。挑战小猪 与具有第3、4、9和10个基因的轮状病毒重组体 SB-1A病毒和DS-1病毒的其余7个基因被开发出来 腹泻和脱落病毒。

Continued efforts have been made to delineate the genetic mechanisms underlying virulence of rotavirus in the newborn gnotobiotic piglet model. A single gene substitution reassortant that had the 1st, 2nd, 5th, 6th, 7th, 8th, or 11th gene from human rotavirus DS-1 strain (which does not induce productive infection or diarrhea in gnotobiotic piglets) and the remaining ten genes from porcine rotavirus SB-1A strain (which consistently induces diarrhea in piglets) induced diarrhea in piglets that was associated with virus shedding. However, piglets challenged with a single gene substitution reassortant that had the VP3 gene, or VP4 gene, or VP7 gene, or NS-28 gene of DS-1 virus and the remaining ten genes from porcine SB-1A virus failed to develop illness or shed virus. Thus, we demonstrated that the 3rd, 4th, 9th (VP7), or 10th (NS28) gene each play an important role in virulence of rotavirus infection in piglets. Piglets challenged with a rotavirus reassortant that had the 3rd, 4th, 9th, and 10th genes of SB-1A virus and the remaining seven genes from DS-1 virus developed diarrhea and shed virus.