Mechanisms of vesicular stomatitis virus-induced cytopathic effects

Baxt, Barry; Bablanian, Rostom

doi:10.1016/0042-6822(76)90167-7

Cited by 49 publications

(5 citation statements)

References 15 publications

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“…In their case mouse myeloma cells, MPC-11, were used. There is evidence that the kinetics of inhibition of RNA synthesis is different in different cell lines (Baxt & Bablanian, 1976; Week & Wagner, 1978).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of ribonucleic acid accumulation in mouse L cells infected with vesicular stomatitis virus requires viral ribonucleic acid transcription

Wu¹,

Lucas‐Lenard²

1980

Biochemistry

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The accumulation of ribonucleic acid (RNA) in mouse L-929 cells infected with temperature-sensitive mutants of vesicular stomatitis virus or ultraviolet- (UV-) irradiated virus was studied. At the permissive temperature (30 degrees C infection by all mutants resulted in an inhibition of cellular RNA accumulation. At the nonpermissive temperature (40 degrees C) mutants G114 (I) and G22 (II) failed to inhibit RNA accumulation, but mutants G11 (I), O52 (II), G31 (III), G33 (III), G41 (IV), W10 (IV), O45 (V), and O110 (V) were still active in this respect. In most cases the accumulation of 28S and 18S mature rRNA was inhibited to a greater extent than the synthesis of the 45S rRNA precursor. UV irradiation of wild type virus considerably reduced its capacity to inhibit cellular RNA synthesis. The target size for inactivation of this capacity of the virus was approximately 17% of the viral genome or that corresponding to the N gene. These results indicate that the virion proteins themselves are incapable of inhibiting cellular RNA synthesis and that transcription of approximately 17% of the genome is required. Expression of RNA synthesis inhibition also requires some function of virion NS protein in addition to its transcriptase activity.

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Section: Discussionmentioning

confidence: 99%

Inhibition of ribonucleic acid accumulation in mouse L cells infected with vesicular stomatitis virus requires viral ribonucleic acid transcription

Wu¹,

Lucas‐Lenard²

1980

Biochemistry

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“…(7) In addition to host protein synthesis other cell functions also change: RNA synthesis is inhibited, the synthesis of lipids is enhanced and there are morphological changes in the infected cell, resulting in celldeath [1][2][3]19]. All these alterations are known as the cytopathic effect [3,2]; it is not known if all have a common origin.…”

Section: *On Leave Of Absence From Institute De Bioqu~mica Dementioning

confidence: 99%

The inhibition of cell functions after viral infection A proposed general mechanism

Carrasco

1977

FEBS Letters

128

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“…Inhibition of host-cell protein synthesis following infection with vesicular stomatitis virus has been well documented (Mudd & Summers, 1970; Wertz & Youngner, 1972;Baxt & Bablanian, 1976;McAllister & Wagner, 1976; Otto & Lucas-Lenard, 1980). This postinfection inhibition of protein synthesis appears to involve two phenomena: (i) a switch from host-cell protein synthesis to predominantly VSV protein synthesis and (ii) a linear decrease with time in overall protein synthesis reaching levels of 50-70% inhibition by 4 h postinfection (Wertz & Youngner, 1972;McAllister & Wagner, 1976).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of translation in lysates of mouse L cells infected with vesicular stomatitis virus: presence of a defective ribosome-associated factor

Thomas¹,

Wagner²

1983

Biochemistry

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Lysates of L cells infected for 4 h with vesicular stomatitis virus were inhibited in their in vitro translational activity to about the same extent as protein synthesis was inhibited in vivo in infected L cells. Inhibition of translation occurred at the level of the ribosome as determined by reciprocal cross-reconstitution studies with polyribosomes and postribosomal supernatant fractions isolated from virus-infected and mock-infected cells. Inhibition of protein synthesis in reconstituted lysates of virus-infected cells was found to be at the level of initiation of translation as evidenced by reduction in incorporation into acid-precipitable proteins of formylatable [35S]methionine. Ribosomes from virus-infected and mock-infected cells were exposed to 0.5 M KCl and fractionated by centrifugation into salt-washed polyribosomes and supernatant fractions containing ribosome-associated proteins; reciprocal reconstitution of translational activity by a mixing of salt-washed polyribosomes and ribosome-associated proteins revealed that the defect in initiation of translation was in the ribosome-associated proteins released by salt wash from the infected-cell ribosomes. Differential ammonium sulfate precipitation of the supernatant ribosome-associated proteins from virus-infected and mock-infected cells indicated by reciprocal reconstitution studies that the defective ribosomal initiation factor(s) was (were) present primarily in the 0-40% ammonium sulfate fraction that is considered to contain primarily eIF-3 and eIF-4B. These results are similar to those found in earlier studies of defective initiation factors responsible for impaired protein synthesis in cells infected with plus-strand viruses quite different from the rhabdovirus studied in these experiments.

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Mechanisms of vesicular stomatitis virus-induced cytopathic effects

Cited by 49 publications

References 15 publications

Inhibition of ribonucleic acid accumulation in mouse L cells infected with vesicular stomatitis virus requires viral ribonucleic acid transcription

Inhibition of ribonucleic acid accumulation in mouse L cells infected with vesicular stomatitis virus requires viral ribonucleic acid transcription

The inhibition of cell functions after viral infection A proposed general mechanism

Inhibition of translation in lysates of mouse L cells infected with vesicular stomatitis virus: presence of a defective ribosome-associated factor

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