Replicative form of Encephalomyocarditis Virus Ribonucleic Acid

Montagnier, Luc; Sanders, F. K.

doi:10.1038/199664a0

Cited by 214 publications

(57 citation statements)

References 30 publications

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“…This may reflect a truly geometric mechanism, in which each progeny RNA molecule is able to act as a template for new molecules. This conclusion is supported by the observations that the proportion of poliovirus recombinants increases during the growth cycle (Ledinko, 1963), and that more than one molecule per cell of the RNA of the closely similar EMC virus can exist in double-stranded form (Montagnier & Sanders, 1963). The underlying mechanism, however, may be no more than pseudogeometric.…”

Section: Discussionsupporting

confidence: 67%

The Kinetics of the Appearance of Poliovirus Ribonucleic Acid

Cooper

1964

Journal of General Microbiology

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SUMMARYOne-step growth conditions were used in which cells began replication of poliovirus RNA almost synchronously, and in which factors limiting the rate of replication appeared to be absent. RNA of uneclipsed virus was destroyed by using light-sensitive inocida. Under these conditions, ribonuclease-sensitive infective RNA was detectable in unchanged amount for the first 2 hr of infection, at which time replication began abruptly; the increase of poliovirus RNA was geometrical for a further 1-2 hr.

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Section: Discussionsupporting

confidence: 67%

The Kinetics of the Appearance of Poliovirus Ribonucleic Acid

Cooper

1964

Journal of General Microbiology

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“…It has been shown that 2C and a cellular protein (p38) bind to the minus-strand 3Ј stem-loop (25,391,392), and this may act to destabilize the RF molecule. The possibility of involvement of either a cellular helicase or a nuclear protein has also been suggested, since the RF is infectious when transfected into whole cells (317) but not when transfected into enucleated cells (322). The elongation of the plus strand by 3D pol also occurs by an unknown mechanism.…”

Section: Infectious Cyclementioning

confidence: 99%

Foot-and-Mouth Disease

2004

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Foot-and-mouth disease (FMD) is a highly contagious disease of cloven-hoofed animals. The disease was initially described in the 16th century and was the first animal pathogen identified as a virus. Recent FMD outbreaks in developed countries and their significant economic impact have increased the concern of governments worldwide. This review describes the reemergence of FMD in developed countries that had been disease free for many years and the effect that this has had on disease control strategies. The etiologic agent, FMD virus (FMDV), a member of the Picornaviridae family, is examined in detail at the genetic, structural, and biochemical levels and in terms of its antigenic diversity. The virus replication cycle, including virus-receptor interactions as well as unique aspects of virus translation and shutoff of host macromolecular synthesis, is discussed. This information has been the basis for the development of improved protocols to rapidly identify disease outbreaks, to differentiate vaccinated from infected animals, and to begin to identify and test novel vaccine candidates. Furthermore, this knowledge, coupled with the ability to manipulate FMDV genomes at the molecular level, has provided the framework for examination of disease pathogenesis and the development of a more complete understanding of the virus and host factors involved

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“…However, the double-stranded Rf of picornavirus RNA has been shown to be infectious by transfection, by e.g. Montagnier & Sanders (1963), and could therefore be contributing to the infectivity of microinjected total infected cell RNA. Any contribution would have to be small since the Rf component does not usually exceed 50~ of FMDV RNA in an infected cell, and, * Particle number was estimated from A260 of the virus suspension assuming 1.0 unit contains 9.6 x 10 ~2 virus particles (Rueckert, 1976).…”

Section: The Replicative Form Of Fmdv Is Less Infectious Than 35s _rnmentioning

confidence: 99%