Vesicular Stomatitis Virus Maturation Sites in Six Different Host Cells

Zee, Y. C.; Hackett, Adeline J.; Talens, L. T.

doi:10.1099/0022-1317-7-2-95

Cited by 50 publications

(23 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Examination of ultrathin sections in a transmission electron microscope showed that virus particles matured at the plasma membrane as reported previously by many investigators (5,6,9). Bullet-shaped virus particles were observed to be attached to the plasma membrane (Fig.…”

Section: Resultssupporting

confidence: 80%

Comparative Studies on Cytopathic Effects Induced by Vesicular Stomatitis Virus in Two Cell Types

Nishiyama

Ito

Shimokata

et al. 1977

Microbiology and Immunology

View full text Add to dashboard Cite

Infection of mouse L cells with vesicular stomatitis virus (VSV) leads to an extensive cell fusion, while porcine kidney stable (PS) cells infected with VSV show only cell rounding. Therefore, comparative morphological studies on the infection of the two cell lines were carried out using a transmission or scanning electron microscope and an immunofluorescence microscope. PS cells infected with VSV contrasted to L cells infected with the same virus in the following two points; (1) the principal site of VSV maturation was the intracytoplasmic vacuolar membrane in PS cells and the plasma membrane in L cells. However, it was found that viral glycoprotein was present on the cell surface of infected PS cells; (2) the morphological changes at the cell surface of infected PS cells occurred much earlier and were severer than those at the cell surface of infected L cells. From these observations, we discuss the possibility that the surface membrane of PS cells is too sensitive to the VSV-induced cell damage to cause cell fusion.Cultures cells infected with cytocidal viruses undergo various cytopathological alterations, and those virus-induced changes termed cytopathic effects (c.p.e.) have been studied in many virus-cell system by means of morphological and biochemical analyses (1). Vesicular stomatitis virus (VSV) is one of the best known cytocidal viruses, and VSV-induced c.p.e. in several cell lines has been described (2-4, 7, 8).In monolayers of certain cell lines infected with VSV, marked polykaryocyte formation can be observed, while only cell rounding can be observed in other cell lines. In a previous report, we described that infection of porcine kidney stable (PS) cells with VSV caused only cell rounding without forming any polykaryocytes although PS cells underwent rapid cell fusion following co-cultivation with VSV-infected L cells, and it remained unclear why PS cells infected with VSV did not show any cell fusion (7).In the present communication, we describe results of a morphological comparison between mouse L cells and PS cells infected with VSV. Parallel studies were done by means of the light microscope, transmission, and scanning electron microscopes.

show abstract

Section: Resultssupporting

confidence: 80%

Comparative Studies on Cytopathic Effects Induced by Vesicular Stomatitis Virus in Two Cell Types

Nishiyama

Ito

Shimokata

et al. 1977

Microbiology and Immunology

View full text Add to dashboard Cite

show abstract

“…Several investigators have observed intracellular vacuoles that appeared during virus assembly (Mussgay & Weibel, 1963;David-West & Labzoffsky, 1968;Zajac & Hummeler, 1970;Zee et al, 1970). Schulze & Liebermann (1966) and Hackett et al (1968) described both vacuole formation and mitochondrial swelling in cells infected with wt VSV.…”

Section: Introductionmentioning

confidence: 99%

Cytopathic Effects in Mouse Neuroblastoma Cells during a Non-permissive Infection with a Mutant of Vesicular Stomatitis Virus

Dille

Hughes

Johnson

et al. 1981

Journal of General Virology

View full text Add to dashboard Cite

SUMMARYMorphological changes were extensive following infection of murine neuroblastoma N-18 cells with a temperature-sensitive (ts) mutant of vesicular stomatitis virus (VSV), G31 (complementation group III), and incubation at 39 °C, a non-permissive condition for virion maturation. Incubation for 24 h after infection resulted in extensive morphological degeneration of mitochondria with over 80 % of the mitochondria having degenerated. Mitochondrial function, as determined by Janus green B supravital staining, was reduced by 81% from that in uninfected cells. Cellular ATP levels were reduced by 50% 12 h after infection. Mitochondrial degeneration still occurred in infected cells after the inactivation of lysosomes with chloroquine. Extensive cell fusion and cytoplasmic vacuole formation also occurred during the non-permissive infection with ts G31. Loss of plasma membrane integrity was not the cause of vacuole formation since 90 % of the cells were able to exclude trypan blue 24 h after infection, nor were the vacuoles the result of inactivation of the mitochondria since cyanide-poisoned cells did not form vacuoles. The cytopathic alterations observed in N-18 cells during the non-permissive infection of N-18 cells with ts G31 did not occur during the non-permissive infection of N-18 cells with ts Gll (I), ts G41 (IV), or u.v.-inactivated ts G31. However, the non-permissive infection with ts O45(V) led to mitochondrial degeneration and cytoplasmic vacuole formation, but no cell fusion occurred. These results are discussed in light of the ultrastructural features previously observed in the central nervous system of mice infected with ts G31 and cells in culture infected with wild-type VSV.

show abstract

“…Vesicular stomatitis virus (VSV) is an RNA-containing, enveloped virus that matures by budding through its host cell's plasma membrane (1,2). The areas of plasma membrane where budding occurs, and the viral membrane envelope, contain proteins specified by the viral genome as well as lipids and glycolipids of cellular origin (3,4).…”

mentioning

confidence: 99%

Carbohydrate Composition of the Membrane Glycoprotein of Vesicular Stomatitis Virus Grown in Four Mammalian Cell Lines

Etchison

Holland

1974

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

The carbohydrate composition of the membrane glycoprotein of-vesicular stomatitis virus has been determined for virus grown in four different mammalian cell lines. The glycoprotein contains mannose, galactose, N-acetylglucosamine, and neuraminic acid as the major carbohydrate components, whereas N-acetylgalactosamine and fucose are present in lesser amounts. Vesicular stomatitis virus (VSV) is an RNA-containing, enveloped virus that matures by budding through its host cell's plasma membrane (1, 2). The areas of plasma membrane where budding occurs, and the viral membrane envelope, contain proteins specified by the viral genome as well as lipids and glycolipids of cellular origin (3, 4). The envelope of VSV contains two protein species: a membrane matrix protein and a glycoprotein (which forms spike-like projections from the viral envelope).The glycoprotein -has an apparent molecular weight of 67,000 (5) and we show elsewhere that when the virus is grown in BHK21 cells, it contains two major oligosaccharide chains with molecular weights of 3000-3400 which represent approximately 10% of the glycoprotein by weight (6). Since the genome of VS virus is not sufficiently complex to specify the many glycosyl transferases which would be required to synthesize these oligosaccharide moieties, most of these enzymes, if not all, must be supplied by the host cell in which the virus replicates. Studies by Burge and Huang (7) indicate that the size of the oligosaccharide chains of purified VSV may differ when it is grown in Chinese hamster ovary cells rather than chick embryo fibroblasts. This difference was attributed to differences in sialic acid content. The relative distribution of the carbohydrate components of purified VSV grown in mouse fibroblasts has been reported to differ from that in chick embryo fibroblasts (8). The contributions of the virus glycolipid to these differences is not apparent, however, since these comparisons were not performed with the isolated glycoproteins.The oligosaccharide moieties of glycoproteins in mammalian cells appear to be synthesized by the sequential addition of monosaccharides to the polypeptide structure. A battery of highly specific glycosyl transferases and compartmentalization of these enzymes are most likely instrumental in specifying the oligosaccharide structure (9). Several studies indicate that polypeptide structure may determine the glycosylation sites (10-13) and that the transferase which adds the first monosaccharide to these sites in the polypeptide may exhibit a stringent requirement for its polypeptide substrate (14). It is not known, however, to what extent, if any, the polypeptide structure may influence the oligosaccharide structure. It is known that the glucosyl transferase involved in collagen biosynthesis, which transfers glucose to galactose bound 0-glycosidically to hydroxylsine, requires the free e-amino group of the hydroxylysine residue (15). This indeed suggests that the influence of the polypeptide structure may extend beyond the biosynthesis of the...

show abstract

Vesicular Stomatitis Virus Maturation Sites in Six Different Host Cells

Cited by 50 publications

References 5 publications

Comparative Studies on Cytopathic Effects Induced by Vesicular Stomatitis Virus in Two Cell Types

Comparative Studies on Cytopathic Effects Induced by Vesicular Stomatitis Virus in Two Cell Types

Cytopathic Effects in Mouse Neuroblastoma Cells during a Non-permissive Infection with a Mutant of Vesicular Stomatitis Virus

Carbohydrate Composition of the Membrane Glycoprotein of Vesicular Stomatitis Virus Grown in Four Mammalian Cell Lines

Contact Info

Product

Resources

About