Cathomen T, Mrkic B, Spehner D, Drillien R, Naef R, Pavlovic J, Aguzzi A, Billeter M A, Cattaneo R
Institut für Molekularbiologie, Abt. I, Universität Zürich, Hönggerberg, 8093 Zürich, Switzerland.
EMBO J. 1998 Jul 15;17(14):3899-908. doi: 10.1093/emboj/17.14.3899.
Measles viruses (MV) can be isolated from the brains of deceased subacute sclerosing panencephalitis patients only in a cell-associated form. These viruses are often defective in the matrix (M) protein and always seem to have an altered fusion protein cytoplasmic tail. We reconstituted a cell-free, infectious M-less MV (MV-DeltaM) from cDNA. In comparison with standard MV, MV-DeltaM was considerably more efficient at inducing cell-to-cell fusion but virus titres were reduced approximately 250-fold. In MV-DeltaM-induced syncytia the ribonucleocapsids and glycoproteins largely lost co-localization, confirming the role of M protein as the virus assembly organizer. Genetically modified mice were inoculated with MV-DeltaM or with another highly fusogenic virus bearing glycoproteins with shortened cytoplasmic tails (MV-Delta(tails)). MV-DeltaM and MV-Delta(tails) lost acute pathogenicity but penetrated more deeply into the brain parenchyma than standard MV. We suggest that enhanced cell fusion may also favour the propagation of mutated, assembly-defective MV in human brains.
仅能以细胞相关形式从亚急性硬化性全脑炎患者死亡后的大脑中分离出麻疹病毒(MV)。这些病毒的基质(M)蛋白常常存在缺陷,且融合蛋白的细胞质尾巴似乎总是发生了改变。我们利用互补DNA重构了一种无细胞的、具有感染性的缺失M蛋白的MV(MV-DeltaM)。与标准MV相比,MV-DeltaM在诱导细胞间融合方面效率显著更高,但病毒滴度降低了约250倍。在MV-DeltaM诱导形成的多核巨细胞中,核糖核蛋白和糖蛋白在很大程度上失去了共定位,这证实了M蛋白作为病毒装配组织者的作用。用MV-DeltaM或另一种带有缩短细胞质尾巴糖蛋白的高融合性病毒(MV-Delta(tails))接种基因改造小鼠。MV-DeltaM和MV-Delta(tails)失去了急性致病性,但比标准MV更深入地渗透到脑实质中。我们认为,增强的细胞融合可能也有利于突变的、装配缺陷的MV在人脑中的传播。