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Journal ArticleDOI

Defective Virions of Reovirus

01 Aug 1970-Journal of Virology (American Society for Microbiology)-Vol. 6, Iss: 2, pp 226-236
TL;DR: The simplest explanation of these results was that stock virus was comprised of two populations of virions, one of which was infectious, whereas the other was not itself infectious and could replicate only in cells coinfected with an H particle virion.
Abstract: When purified preparations of stock reovirus, type 3, were digested with chymotrypsin, the virions were converted into two different types of particle. These new particles could be separated from each other by isopycnic centrifugation in cesium chloride gradients. One particle banded at a buoyant density of 1.43 g/cm3, the other at a density of 1.415 g/cm3. The former particle is termed the heavy (H) particle, the latter is the light (L) particle. The ratio of H/L particles varied between 0.5 and 0.25 in various purified preparations of virus. In electron micrographs, both H and L particles had the appearance and dimensions of viral cores. H particles were infectious for L cells. When plaques formed by stock virus, or by H particles, were picked and propagated in L cells, the majority of the clones gave rise only to H particles on chymotrypsin digestion. On continued serial passage of the clones, virions containing L particles again appeared in the progeny. The simplest explanation of these results was that stock virus was comprised of two populations of virions. One type of virion which contained H particles was infectious, whereas the other, which contained L particles, was not itself infectious and could replicate only in cells coinfected with an H particle virion. Added weight was given to this hypothesis by two observations. First, a small but definite separation of H and L virions could be achieved by isopycnic centrifugation in a gradient of cesium chloride. Second, L particles and virions containing L particles were both shown to lack the largest of the ten segments of double-stranded ribonucleic acid genome. Thus, L particle virions have defective genomes.
Citations
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Book ChapterDOI
TL;DR: Defective interfering virus (DI) particles represent a major controlling element of virus replication and only amplify to interfering levels when the parent helper vims is abundant.
Abstract: Defective interfering virus (DI) particles represent a major controlling element of virus replication. They are constantly generated at low levels by infectious virus and only amplify to interfering levels when the parent helper vims is abundant. This autointerference phenomenon, as it was called when first discovered, is achieved by rearrangements and deletions of the standard virus genome such that the resulting “incomplete form” of the virus can preferentially replicate.

275 citations

Journal ArticleDOI
01 Sep 1969-Virology
TL;DR: Treatment of penton antigen with pyridine releases free vertex capsomers which are immunologically and morphologically intact and have the ability to induce cytopathic changes in KB-cell cultures.

261 citations

Book ChapterDOI
01 Jan 1977
TL;DR: Defective interfering particles were discovered three decades ago by von Magnus using the influenza virus system and a great deal was learned from their physiological interactions with the host and from their interference with the multiplication of “infectious” standard virus.
Abstract: Defective interfering (DI) particles were discovered three decades ago by von Magnus (1947) using the influenza virus system. He called them “incomplete” or “immature” particles. Even though they could not be isolated or characterized biochemically, a great deal was learned about them from their physiological interactions with the host and from their interference with the multiplication of “infectious” standard virus (Gard and von Magnus, 1947; Bernkopf, 1950; von Magnus, 1951). Reviews by Henle (1950), by von Magnus (1954), and by Schlesinger (1959) on viral interference discuss the earlier work on this particular homologous interference caused by incomplete virus.

226 citations

Journal ArticleDOI
TL;DR: The universality and diversity of defective viral genomes during infections are highlighted and their predicted role in maintaining a fit virus population, their impact on human and animal health, and their potential to be harnessed as antiviral tools are discussed.
Abstract: Viruses survive often harsh host environments, yet we know little about the strategies they utilize to adapt and subsist given their limited genomic resources. We are beginning to appreciate the surprising versatility of viral genomes and how replication-competent and -defective virus variants can provide means for adaptation, immune escape and virus perpetuation. This Review summarizes current knowledge of the types of defective viral genomes generated during the replication of RNA viruses and the functions that they carry out. We highlight the universality and diversity of defective viral genomes during infections and discuss their predicted role in maintaining a fit virus population, their impact on human and animal health, and their potential to be harnessed as antiviral tools.

193 citations

Journal ArticleDOI
TL;DR: An internal region of the poliovirus genome was identified whose translation is required in cis; failure to translate this region was shown to inhibit RNA replication, suggesting a coupling between translation and RNA replication could provide a late proofreading mechanism that enables poliov virus, and possibly many other RNA viruses, to prevent the replication of defective genomes.
Abstract: The replication of poliovirus RNA genomes containing amber mutations was studied to test whether viral proteins provided in trans could rescue the replication of an RNA genome that could not be completely translated itself. Mutants containing amber codons at different positions in the genome displayed vastly different abilities to be rescued by wild-type proteins provided by a helper genome. Amber-suppressing cell lines were used to ensure that the defects in the amber mutants arose from their failure to be translated, not from defects in RNA sequence or structure. An internal region of the poliovirus genome was identified whose translation is required in cis; failure to translate this region was shown to inhibit RNA replication. This coupling between translation and RNA replication could provide a late proofreading mechanism that enables poliovirus, and possibly many other RNA viruses, to prevent the replication of defective genomes.

192 citations

References
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Journal ArticleDOI
01 Dec 1969-Virology
TL;DR: The molecular weights of the three size classes of capsid polypeptides are such that they are probably coded by monocistronic messenger RNA molecules transcribed from the L, M, and S segments of reovirus genome RNA.

630 citations


"Defective Virions of Reovirus" refers background or methods in this paper

  • ...(17) describe cores obtained by a similar method as having a density of 1....

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  • ...Both H and L particles had the appearance and dimensions of viral cores (8, 14, 17)....

    [...]

  • ...When purified reovirus is digested with chymotrypsin, the capsomeres are removed leaving the core particles which can be identified in the electron microscope (3, 14, 17, 18)....

    [...]

Book ChapterDOI
TL;DR: This chapter describes the experimental conditions required for the production of fully active and incomplete influenza virus and discusses the various hypotheses about the mechanism responsible for the formation of incomplete virus along with the nature and origin of the virus.
Abstract: Publisher Summary This chapter describes the experimental conditions required for the production of fully active and incomplete influenza virus. Well-adapted laboratory strains of fully active virus are grown from dilute seeds and harvested when the virus activity becomes maximal. The formation of large amounts of incomplete influenza virus has been observed in embryonated eggs and in a number of other host-cell systems. Incomplete influenza virus is produced also in tissue cultures seeded with large concentrations of Standard virus. Incomplete virus particles are practically undistinguishable from the fully active virus in size, shape, and biologic surface characteristics. They differ from the fully active particles by having a lower sedimentation constant, by the apparent lack of infectivity, and by their capacity to interfere with and inhibit the propagation of the infective virus. The chapter also discusses the various hypotheses about the mechanism responsible for the formation of incomplete virus, along with the nature and origin of the virus.

340 citations

Journal ArticleDOI
TL;DR: Double-stranded ribonucleic acid extracted from purified reoviruses of all three serotypes and from type 3 virus-infected cells was analyzed by polyacrylamide gel electrophoresis and calculated that each RNA includes 10 segments.
Abstract: Double-stranded ribonucleic acid (RNA) extracted from purified reoviruses of all three serotypes and from type 3 virus-infected cells was analyzed by polyacrylamide gel electrophoresis. It was calculated that each RNA includes 10 segments: 3 large, 3 intermediate, and 4 small fragments corresponding to molecular weights of about 2.5, 1.4, and 0.8 × 106 daltons, respectively, or a total of 15 × 106 daltons.

257 citations


"Defective Virions of Reovirus" refers background in this paper

  • ...Since the genome of reovirus is known to contain 10 segments of dsRNA which can be resolved by electrophoresis on pDlyacrylamide gels (15, 23), it was at least possible to determine whether or not both particles contained a full complement of dsRNA....

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Journal ArticleDOI
01 Dec 1969-Virology
TL;DR: The enzyme present in reovirus particles is thus a novel RNA transcriptase which transcribes double-stranded RNA in a manner analogous to that by which DNA-dependent RNA polymerase transcribes DNA.

236 citations