Plattet, PhilippePhilippePlattetRivals, Jean-PaulJean-PaulRivalsZuber, BenoîtBenoîtZuber0000-0001-7725-5579Brunner, Jean-MarcJean-MarcBrunnerZurbriggen, AndreasAndreasZurbriggenWittek, RiccardoRiccardoWittek2024-10-232024-10-232005-07-05https://boris-portal.unibe.ch/handle/20.500.12422/137200The wild-type A75/17 canine distemper virus (CDV) strain induces a persistent infection in the central nervous system but infects cell lines very inefficiently. In contrast, the genetically more distant Onderstepoort CDV vaccine strain (OP-CDV) induces extensive syncytia formation. Here, we investigated the roles of wild-type fusion (F(WT)) and attachment (H(WT)) proteins in Vero cells expressing, or not, the canine SLAM receptor by transfection experiments and by studying recombinants viruses expressing different combinations of wild-type and OP-CDV glycoproteins. We show that low fusogenicity is not due to a defect of the envelope proteins to reach the cell surface and that H(WT) determines persistent infection in a receptor-dependent manner, emphasizing the role of SLAM as a potent enhancer of fusogenicity. However, importantly, F(WT) reduced cell-to-cell fusion independently of the cell surface receptor, thus demonstrating that the fusion protein of the neurovirulent A75/17-CDV strain plays a key role in determining persistent infection.en500 - Science::570 - Life sciences; biology600 - Technology::610 - Medicine & healtharticle10.7892/boris.747941589378310.1016/j.virol.2005.04.012