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Department of Microbiology, University of Geneva, C.M.U., 9 avenue de Champel, 1211 Geneva 4, Switzerland
and1 Division of Virology and Molecular Biology, St Jude Children's Research Hospital, Memphis, Tennessee, U.S.A.
The fate of the haemagglutinin-neuraminidase glycoprotein (HN) of Sendai virus in three types of infection was studied by measuring its sensitivity to endoglycosidase H and its rate of appearance and turnover at the cell surface. HN behaved differently in the three types of infection. When highly expressed at the surface, as in a lytic standard virus infection, HN accumulated at the surface in a stable form (half-life of disappearance from the surface » 10 h). When moderately expressed, as in a non-lytic standard virus plus defective interfering virus infection, HN reached the membrane normally, but turned over rapidly (half-life about 2 h) and was re-internalized. When poorly expressed, as in long-term persistent infection, HN did not reach the cell surface and appeared to be degraded before reaching it. In contrast to HN, the other viral glycoprotein, F0, exhibited a similar turnover rate at the cell surface in the three situations. However, when compared to surface expression in standard virus-infected cells under standardized conditions, F0 surface expression in persistently infected cells was reduced. This reduction correlates with a decreased maturation rate in these cells.
Keywords: Sendai virus, HN, persistent infection
Received 1 November 1984;
accepted 15 January 1985.
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