Galbraith S E, Tiwari A, Baron M D, Lund B T, Barrett T, Cosby S L
Institute for Animal Health, Pirbright Laboratory, Pirbright, Woking, Surrey GU24 ONF, United Kingdom.
J Virol. 1998 Dec;72(12):10292-7. doi: 10.1128/JVI.72.12.10292-10297.1998.
There is evidence that CD46 (membrane cofactor protein) is a cellular receptor for vaccine and laboratory-passaged strains of measles virus (MV). Following infection with these MV strains, CD46 is downregulated from the cell surface, and consequent complement-mediated lysis has been shown to occur upon infection of a human monocytic cell line. The MV hemagglutinin (H) protein alone is capable of inducing this downregulation. Some wild-type strains of MV fail to downregulate CD46, despite infection being prevented by anti-CD46 antibodies. In this study we show that CD46 is also downregulated to the same extent by wild-type, vaccine, and laboratory-passaged strains of rinderpest virus (RPV), although CD46 did not appear to be the receptor for RPV. Expression of the RPV H protein by a nonreplicating adenovirus vector was also found to cause this downregulation. A vaccine strain of peste des petits ruminants virus caused slight downregulation of CD46 in infected Vero cells, while wild-type and vaccine strains of canine distemper virus and a wild-type strain of dolphin morbillivirus failed to downregulate CD46. Downregulation of CD46 can, therefore, be a function independent of the use of this protein as a virus receptor.
有证据表明,CD46(膜辅因子蛋白)是麻疹病毒(MV)疫苗株和实验室传代株的细胞受体。感染这些MV毒株后,CD46从细胞表面下调,并且已证明在感染人单核细胞系时会发生补体介导的细胞裂解。单独的MV血凝素(H)蛋白就能诱导这种下调。一些MV野生型毒株尽管抗CD46抗体可预防感染,但却无法下调CD46。在本研究中,我们表明,牛瘟病毒(RPV)的野生型、疫苗株和实验室传代株也能将CD46下调至相同程度,尽管CD46似乎不是RPV的受体。还发现,非复制型腺病毒载体表达RPV H蛋白也会导致这种下调。小反刍兽疫病毒疫苗株在感染的Vero细胞中会使CD46略有下调,而犬瘟热病毒的野生型和疫苗株以及海豚麻疹病毒野生型毒株则无法下调CD46。因此,CD46的下调可能是一种与将该蛋白用作病毒受体无关的功能。