Multiplicity reactivation and marker rescue with vaccinia virus

Abel, Pamela

doi:10.1016/0042-6822(62)90150-2

Cited by 54 publications

(23 citation statements)

References 18 publications

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“…classical multiplicity reactivation (MR) . Such an MR was already shown for heavily U .V .-irradiated vaccinia virus (Abel 1962) . The relative part of both phenomena in ME is currently not amenable to measurement .…”

supporting

confidence: 62%

Multiplicity Effect on the Survival of Ultra-violet-irradiatedHerpes SimplexVirus

Coppey

Nocentini

1973

International Journal of Radiation Biology and Related Studies

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supporting

confidence: 62%

Multiplicity Effect on the Survival of Ultra-violet-irradiatedHerpes SimplexVirus

Coppey

Nocentini

1973

International Journal of Radiation Biology and Related Studies

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“…As expected, due to variation in the methods used (e.g., varied strain virulence, adaptation to the host (Overman & Sharp, 1959), virus disruption due to experimental methods (Dales, 1963), topographical effects of host cells (Abel, 1962), and variance in the virus and pock or plaque counts), a range of estimates has been reported. Only Parker and Rivers (1938) and Sprunt, Marx, and Beard (1940) reported a count of vaccinia virus per infectious unit that did not include 20 virus or less.…”

Section: Studies Of the Infectious Unitmentioning

confidence: 88%

The Infectious Dose of Variola (Smallpox) Virus

et al. 2004

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Quantitative estimation of an individual's risk of infection due to airborne pathogens requires knowledge of the pathogen's infectious dose, in addition to estimates of the pathogen's airborne concentration and the person's exposure duration. Based on our review of the published literature on poxvirus infection, we conclude that the infectious dose of variola (smallpox) virus is likely one virus particle and that infection can be initiated in either the upper respiratory tract or pulmonary region. Studies of airborne transmission of poxvirus in monkeys and rabbits show that primary infection can occur in both regions of the respiratory tract. A quantitative study of poxvirus inhalation transmission in rabbits indicates that the deposition of one pock-forming unit (PFU) carried on respirable particles can cause infection. Findings in both in vitro and in vivo studies of the number of virus particles comprising a PFU are consistent with a "one-hit" phenomenon-namely, the cellular uptake of just one virus particle can lead to infection of a cell or an area of cell growth, creating a pock (an infected area of cells). Variability in virulence among different virus strains may involve differences inthe probability of infection per virus particle, where a highly virulent strain has a probability close to one of successful infection for each virus particle. In an analogous manner, variability in susceptibility to the same virus strain among different hosts may involve differences in the probability of infection per virus particle across different hosts. Applied Biosafety, 9(3) pp. 118-127

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“…Pock counts on the GAM were made by the method of Westwood, Phipps and Boulter (1957), Plaque assays were based upon the method of Abel (1962) for GF, and of McGlain andHackett (1958, 1959) for all other cells. Details of the techniques are presented in "Results".…”

Section: Methodsmentioning

confidence: 99%

“…This paper reports the results of an investigation of the efficiency of plating and plaque morphology of the u mutants of Gemmell and Fenner (1960) on monolayers of chick fibroblasts prepared by Abel's (1962) method, which involves the inoculation of freshly-prepared cell suspensions which are overlaid after overnight incubation in liquid medium. In addition a survey has been made of the response of several cell lines to the RP« mutants.…”

Section: Introductionmentioning

confidence: 99%

THE HOST RANGE AND PLAQUE MORPHOLOGY OF RABBITPOX VIRUS (RPu+) AND ITS u MUTANTS ON CHICK FIBROBLAST, PK‐2a, AND L929 CELLS

McClain

1965

Aust J Exp Biol Med

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Summary.Rabbitpox virus (RP«+), 18 white pock (u) mutants derived from it and several strains of vaccinia virus were examined in respect to their cytopathology in ehiek embryo fibroblast cultures, and several continuous lines of mammalian cells; PK-2a (pig kidney), L929 (mouse fibroblast), FAF (Chinese hamster fibroblast), AT (Chinese hamster, epithelial), KB (human epithelial), FL (human amnion) and Chang liver (human epithelial). The plaquing characteristics of the viruses, and the capacity to multiply exhibited by those which did not produce plaques, were investigated in chick fibroblast, PK-2a, and L929 cells.Cytopathic changes were characterized by early toxic effects, cellular fusion, and progressive destruction of monolayers, the pattern of changes being a function of specific virus-cell combinations. With input inocula of 1-5 PFU per cell, most of the virus strains and mutants produced toxic changes in most of the epithelial type cells (PK-2a, FL, Chang liver) but not in the fibroblastic cells, and to a very slight degree in KB cells. Three mutants which failed to multiply in PK-2a cells nevertheless produced moderate toxic changes in them.Pronounced fusion of cells was produced in the epithelial type cells, but not in fibroblastic cells, by most of the viruses which multiplied in them, but not by mutants which failed to multiply.All the mutants produced plaques on chick embryo fibroblasts, and these could be distinguished as turbid or clear, and differed in size and in cultural requirements for maximal plating efficiency. A standard plaque assay method is described which gives good plaques with the majority of mutants.Conditions for optimal plaque assays on PK-2a and L929 cells are also described, and several distinctive plaque types were recognized. Some mutants failed to produce plaques on PK-2a or L929 cells, and in all cases except one this was shown to be due to their failure to multiply in the cells concerned.

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Multiplicity reactivation and marker rescue with vaccinia virus

Cited by 54 publications

References 18 publications

Multiplicity Effect on the Survival of Ultra-violet-irradiatedHerpes SimplexVirus

Multiplicity Effect on the Survival of Ultra-violet-irradiatedHerpes SimplexVirus

The Infectious Dose of Variola (Smallpox) Virus

THE HOST RANGE AND PLAQUE MORPHOLOGY OF RABBITPOX VIRUS (RPu+) AND ITS u MUTANTS ON CHICK FIBROBLAST, PK‐2a, AND L929 CELLS

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