Adami C, Pritchard A E, Knauf T, Luo M, Lipton H L
Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, and Evanston Hospital, Illinois 60201, USA.
J Virol. 1998 Feb;72(2):1662-5. doi: 10.1128/JVI.72.2.1662-1665.1998.
The demyelinating process in Theiler's murine encephalomyelitis virus (TMEV) infection in mice requires virus persistence in the central nervous system. Using recombinant TMEV assembled between the virulent GDVII and less virulent BeAn virus cDNAs, we now provide additional evidence supporting the localization of a persistence determinant to the leader P1 (capsid) sequences. Further, recombinant viruses in which BeAn sequences progressively replaced those of GDVII within the capsid starting at the leader NH2 terminus suggest that a conformational determinant requiring homologous sequences in both the VP2 puff and VP1 loop regions, which are in close contact on the virion surface, might underlie persistence.
小鼠感染泰勒氏鼠脑脊髓炎病毒(TMEV)后的脱髓鞘过程需要病毒在中枢神经系统中持续存在。利用在强毒株GDVII和弱毒株BeAn病毒cDNA之间组装的重组TMEV,我们现在提供了额外的证据,支持将持续存在决定簇定位到前导P1(衣壳)序列。此外,从衣壳前导NH2末端开始,BeAn序列逐渐取代GDVII序列的重组病毒表明,一种构象决定簇可能是持续存在的基础,该决定簇需要病毒粒子表面紧密接触的VP2膨松区和VP1环区中的同源序列。