Literature DB >> 3006337

Lack of correlation between the accumulation of plus-strand leader RNA and the inhibition of protein and RNA synthesis in vesicular stomatitis virus infected mouse L cells.

D D Dunigan, S Baird, J Lucas-Lenard.   

Abstract

The inhibition of protein synthesis in mouse L cells infected by vesicular stomatitis virus (VSV) requires expression of two regions (one large and one small) of the viral genome, as determined by target size analysis. The inhibition of host RNA synthesis was also shown to be dependent on expression of two regions of the VSV genome, most likely the same ones. In some cases, such as in cells infected by mutants T1026R1, or tsG41 at 40 degrees, or moderately uv irradiated VSV, only one of the two regions was expressed, yet cellular protein and RNA synthesis was decreased. This suggests that the product of each region of the viral genome can act independently. In these instances the severity of the inhibition was dependent on both the length of the infection period and the multiplicity of infection. The identity of neither gene product is known, but it has been suggested that small product is plus-strand leader RNA. As shown herein, however, there was no correlation between the extent of host macromolecular synthesis inhibition and the quantity of leader RNA in infected cells.

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Year:  1986        PMID: 3006337     DOI: 10.1016/0042-6822(86)90282-5

Source DB:  PubMed          Journal:  Virology        ISSN: 0042-6822            Impact factor:   3.616


  16 in total

Review 1.  Cytopathogenesis and inhibition of host gene expression by RNA viruses.

Authors:  D S Lyles
Journal:  Microbiol Mol Biol Rev       Date:  2000-12       Impact factor: 11.056

2.  Matrix protein and another viral component contribute to induction of apoptosis in cells infected with vesicular stomatitis virus.

Authors:  S A Kopecky; M C Willingham; D S Lyles
Journal:  J Virol       Date:  2001-12       Impact factor: 5.103

3.  Viral transcription is necessary and sufficient for vesicular stomatitis virus to inhibit maturation of small nuclear ribonucleoproteins.

Authors:  D E Crone; J D Keene
Journal:  J Virol       Date:  1989-10       Impact factor: 5.103

4.  Genome RNA terminus conservation and diversity among vesiculoviruses.

Authors:  S T Nichol; J J Holland
Journal:  J Virol       Date:  1987-01       Impact factor: 5.103

5.  The vesicular stomatitis virus matrix protein inhibits NF-κB activation in mouse L929 cells.

Authors:  Andrew J Varble; Christopher D Ried; Warren J Hammond; Kaitlin A Marquis; Matthew C Woodruff; Maureen C Ferran
Journal:  Virology       Date:  2016-09-17       Impact factor: 3.616

6.  Effect of vesicular stomatitis virus matrix protein on host-directed translation in vivo.

Authors:  B L Black; G Brewer; D S Lyles
Journal:  J Virol       Date:  1994-01       Impact factor: 5.103

7.  The role of vesicular stomatitis virus matrix protein in inhibition of host-directed gene expression is genetically separable from its function in virus assembly.

Authors:  B L Black; R B Rhodes; M McKenzie; D S Lyles
Journal:  J Virol       Date:  1993-08       Impact factor: 5.103

8.  Vesicular stomatitis virus in Drosophila melanogaster cells: lack of leader RNA transport into the nuclei and frequent abortion of the replication step.

Authors:  S Dezélée; D Blondel; F Wyers; A M Petitjean
Journal:  J Virol       Date:  1987-05       Impact factor: 5.103

9.  Effect of vesicular stomatitis virus matrix protein on transcription directed by host RNA polymerases I, II, and III.

Authors:  M Ahmed; D S Lyles
Journal:  J Virol       Date:  1998-10       Impact factor: 5.103

10.  Nuclear entry and nucleolar localization of the Newcastle disease virus (NDV) matrix protein occur early in infection and do not require other NDV proteins.

Authors:  M E Peeples; C Wang; K C Gupta; N Coleman
Journal:  J Virol       Date:  1992-05       Impact factor: 5.103

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