Pinschewer Daniel D, Perez Mar, Sanchez Ana B, de la Torre Juan Carlos
Department of Neuropharmacology, The Scripps Research Institute, IMM6, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7895-900. doi: 10.1073/pnas.1332709100. Epub 2003 Jun 13.
A recombinant S segment RNA (Sr) of the prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) where the glycoprotein of vesicular stomatitis virus (VSVG) was substituted for the glycoprotein of LCMV (LCMV-GP) was produced intracellularly from cDNA under the control of a polymerase I promoter. Coexpression of the LCMV proteins NP and L allowed expression of VSVG from Sr. Infection of transfected cells with WT LCMV (LCMVwt) resulted in reassortment of the L segment of LCMVwt with the Sr at low frequency. Isolation of recombinant LCMV (rLCMV) expressing VSVG (rLCMV/VSVG) was achieved by selection against LCMVwt by using a cell line deficient in the cellular protease S1P. This approach was based on the finding that processing of LCMV-GP by S1P was required for virus infectivity. Characterization of protein and RNA expression of rLCMV/VSVG in infected cells confirmed the expected virus genome organization. rLCMV/VSVG caused syncytium formation in cultured cells and grew to approximately 100-fold lower titers than WT virus but, like the parent virus, it persisted in neonatally infected mice without clinical signs of disease.
在聚合酶I启动子的控制下,从cDNA在细胞内产生了原型沙粒病毒淋巴细胞性脉络丛脑膜炎病毒(LCMV)的重组S片段RNA(Sr),其中水泡性口炎病毒(VSVG)的糖蛋白替代了LCMV的糖蛋白(LCMV-GP)。LCMV蛋白NP和L的共表达使得VSVG能从Sr表达。用野生型LCMV(LCMVwt)感染转染细胞会导致LCMVwt的L片段与Sr以低频率重配。通过使用细胞内蛋白酶S1P缺陷的细胞系来筛选对抗LCMVwt,从而实现了表达VSVG的重组LCMV(rLCMV/VSVG)的分离。该方法基于这样一个发现,即病毒感染性需要S1P对LCMV-GP进行加工。对感染细胞中rLCMV/VSVG的蛋白质和RNA表达进行表征,证实了预期的病毒基因组结构。rLCMV/VSVG在培养细胞中引起了合胞体形成,其生长滴度比野生型病毒低约100倍,但与亲本病毒一样,它在新生感染小鼠中持续存在,且无疾病的临床症状。