Defective Particles in BHK Cells Infected with Temperature-Sensitive Mutants of Vesicular Stomatitis Virus

Reichmann, M. E.; Pringle, C. R.; Follett, E. A. C.

doi:10.1128/jvi.8.2.154-160.1971

Cited by 61 publications

(21 citation statements)

References 17 publications

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“…ts Mutants of wild-type strains of the Indiana serotype have been characterized in some detail in genetic (5, 6, 12, 13) and biochemical terms (10,(14)(15)(16); Szildigyi and Pringle and Wunner and Pringle, in preparation).…”

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Isolation and Characterization of Temperature-Sensitive Mutants of Vesicular Stomatitis Virus, New Jersey Serotype

Pringle

Duncan

Stevenson

1971

J Virol

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Forty-eight temperature-sensitive ( ts ) mutants have been isolated from a wild-type strain of the New Jersey serotype of vesicular stomatitis virus (VSV) after exposure to the base analogue mutagen 5-fluorouracil. Of these mutants, 47 have been classified into 6 nonoverlapping complementation groups containing 21, 17, 4, 3, 2, and 1 mutant, respectively (1 mutant remaining unallocated). The ribonucleic acid (RNA) phenotype of 23 of these mutants has been established. Four of the six groups contain one or more mutants unable to synthesize detectable amounts of viral RNA under restrictive conditions (39 C). No complementation was observed in mixed infection with ts mutants from the five established complementation groups of the Indiana serotype of VSV.

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confidence: 99%

Isolation and Characterization of Temperature-Sensitive Mutants of Vesicular Stomatitis Virus, New Jersey Serotype

Pringle

Duncan

Stevenson

1971

J Virol

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“…If subgenomic DNA fragments are generated by replication errors (4) and are themselves replicated, then the apparent serotype-specific distribution of predominant bands could arise from initial random generation of lengths, the predominant size classes being perpetuated through contamination of wild-type virions with seed amounts of defective DNA-containing particles. Defective RNAs synthesized by vesicular stomatitis virus are generated in this way, and an apparent strain specificity can in fact be lost by extensive plaque purification (16,27,34). The observation that Ad5 generated subgenomic DNAs in monkey cells but not in premissive cells allowed rigorous testing of the proposal that in the case of adenovirus-defective genomes the array of predominant sizes is genetically determined.…”

Section: Resultsmentioning

confidence: 99%

“…The latter is the case for vesicular stomatitis virus, which generates defective particles containing subgenomic RNAs with inverted terminal repetitions (23,28,29). For many years, it was thought that different vesicular stomatitis virus strains gave rise to genetically determined classes of defective particles (27,34). It has now been demonstrated by Holland et al (16) that, after careful serial cloning of vesicular stomatitis virus, a random and unpredictable array of defective particles is generated; the particles then breed true in subsequent passages and are enriched.…”

Section: Resultsmentioning

confidence: 99%

Subgenomic viral DNA species synthesized in simian cells by human and simian adenoviruses

Daniell¹

1981

J Virol

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DNA synthesized after infection of simian tissue culture cells (BSC-1 or CV-1) with human adenovirus type 2 or 5 or with simian adenovirus 7 was characterized. It was demonstrated that as much as 40% of the virus-specific DNA in nuclei of infected monkey cells consists of subgenomic pieces. No subgenomic viral DNA species were detected in the nuclei of human (HeLa) cells infected with these adenovirus types. Restriction analysis showed that these short viral DNA molecules contain normal amounts of the sequences from the ends of the viral genome, whereas internal regions are underrepresented. The production of subgenomic DNAs is not correlated with semipermissive infection. Although adenovirus types 2 and 5 are restricted in monkey cells, these cells are fully permissive for simian adenovirus 7. HR404, an adenovirus type 5 mutant which is not restricted in monkey cells, produced the same percentage of subgenomic DNAs as did its wild type (restricted) parent, and coinfection of monkey cells with adenovirus type 5 DNAs. The array of predominant size classes among the heterogeneously sized short DNAs is serotype specific. Extensive plaque purification and comparison of wild-type adenovirus type 5 with several viral mutants indicated that the distribution of aberrant sizes of DNA is characteristic of the virus and not a result of random replicative errors and then enrichment of particular species.

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“…Each of these mutants was plaque purified in Reichmann's laboratory and subsequently passaged by infecting cells with 0.01 to 0.1 PFU/cell to minimize production of DI particles of the ts mutants. ts 31 is a member of complementation group III (11) and ts 41 is a member of complementation group IV (11). Initially, 25-cm2 flasks containing confluent monolayers of BHK-21 cells were infected with dilute passage (--0.1 PFU/cell) ts virus.…”

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confidence: 99%

Comparison of central nervous system disease produced by wild-type and temperature-sensitive mutants of vesicular stomatitis virus

Rabinowitz¹,

Canto²,

Johnson³

1976

Infect Immun

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The pathogenicity of infection produced following intracerebral (i.c.) inoculation of wild-type vesicular stomatitis virus (VSV) or temperature-sensitive (ts) mutants of VSV was compared. ts mutants used were ts 31 (VSV complementation group II) and ts 41 (VSV complementation group IV). The i.c. injection of wild-type VSV in weanling Swiss mice produced a rapidly fatal encephalitis with death of mice in 2 to 3 days. Histopathologically, such mice exhibited minimal changes of encephalitis on light microscopy. In contrast to the highly virulent, rapidly fatal central nervous system (CNS) infection seen after i.c. inoculation of wild-type VSV, infection with ts 31 VSV produced a more slowly progressive CNS infection characterized by hind limb paralysis and death 6 to 9 days after infection. Histopathologically, CNS infection with ts 31 is associated with previously unreported extensive spongiform changes in the gray matter of the spinal cord. The inoculation of ts 41 i.c., on the other hand, did not result in either clinical illness or histopathological changes in the spinal cords or brains of infected mice. The absence of clinical and histopathological lesions following i.c. infection ofts 41 VSV suggests that the capacity to alter the pathogenesis of VSV CNS infection may be a function of only certain ts mutants of VSV.

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Defective Particles in BHK Cells Infected with Temperature-Sensitive Mutants of Vesicular Stomatitis Virus

Cited by 61 publications

References 17 publications

Isolation and Characterization of Temperature-Sensitive Mutants of Vesicular Stomatitis Virus, New Jersey Serotype

Isolation and Characterization of Temperature-Sensitive Mutants of Vesicular Stomatitis Virus, New Jersey Serotype

Subgenomic viral DNA species synthesized in simian cells by human and simian adenoviruses

Comparison of central nervous system disease produced by wild-type and temperature-sensitive mutants of vesicular stomatitis virus

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