Three Variations in the Cell Surface Expression of the Haemagglutinin-Neuraminidase Glycoprotein of Sendai Virus

Abstract

SUMMARYThe fate of the haemagglutinin-neuraminidase glycoprotein (HN) of Sendal 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-lyric 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.

The role of Haemagglutinin-Neuraminidase Glycoprotein Cell Surface Expression in the Survival of Sendai Virus-infected BHK-21 Cells

“…In conclusion, the hypothesis proposed in previous reports (Roux & Waldvogel, 1983;Roux et al, 1984Roux et al, , 1985, that lack of H N cell surface expression was sufficient to allow cell survival, was not verified. This was especially striking in this system since the reduction of H N surface expression achieved using ts 271 was more pronounced than that observed previously following mixed virus infection sufficient for complete cell survival (Roux & Waldvogel, 1983, Roux et al, 1984.…”

“…These proteins form the spikes seen in the virus envelope (Choppin & Compans, 1975). On the other hand, HN cell surface expression was shown to be significantly reduced at the surface of the mixed virus-infected cells, and also was absent at the surface of the long-term persistently infected cells (Roux & Waldvogel, 1983;Roux et aL, 1984Roux et aL, , 1985. Therefore, it was reasonable to assume that lack of insertion of HN in the cell membrane may have abolished the cytopathic effect (c.p.e.)…”

“…As HN cell surface expression is affected by co-infection of standard virus and DI particles (Roux & Waldvogel, 1983 ;Roux et al, 1984Roux et al, , 1985, our first concern was to prepare ts 271 virus stocks free of DI particles by serial plaque purifications (see Methods), and to ensure that the viral nucleocapsids isolated from cells infected with these stocks contained only full-length genome-size RNA (data not shown).…”

“…In an attempt to understand the mechanisms leading to survival of the infected cells and establishment of persistent infection, comparison of standard, standard plus DI (mixed) and persistent virus infections has been made using BHK cells (Roux & Waldvogel, 1981, 1983Roux et al, 1984Roux et al, , 1985. These studies led to the conclusion that the viral glycoproteins were differentially expressed at the surface of the infected cells depending on the type of infection.…”

A Single Amino Acid Change in the Cytoplasmic Domains of Measles Virus Glycoproteins H and F Alters Targeting, Endocytosis, and Cell Fusion in Polarized Madin-Darby Canine Kidney Cells

“…Arrows indicate syncytia. regulate the expression of viral envelope proteins by interaction with viral core proteins have been proposed for Sendai virus and the human immunodeficiency virus (42,43). In contrast, glycoproteins from the simian immunodeficiency virus and simian virus 5 have been found to be internalized even in the presence of viral core proteins (44,45).…”