Comparison of ribonucleotide sequences from the genome of vesicular stomatitis virus and two of its defective interfering particles

Hagen, Frederick S.; Huang, Alice S.

doi:10.1128/jvi.37.1.363-371.1981

Cited by 7 publications

(4 citation statements)

References 26 publications

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“…The basis for the replicative advantage of the larger DI is unknown but it is unlikely to be directly related to stem sizes since this parameter does not affect relative interfering ability in other VSV DI (see previous Section). The presence of different point mutations in each of these two DI RNAs which are not present in standard virus was also reported and is perhaps responsible for this odd behaviour (Hagen and Huang, 1981). The accumulation of point mutations in DI RNAs may be more widespread than hitherto suspected and may also be related to the phenomenon of mutational drift observed in standard virus RNA during DI-mediated virus persistence.…”

Section: Additional Parameters Affecting Vsv DI Interferencementioning

confidence: 83%

Origin and Replication of Defective Interfering Particles

Perrault

1981

Current Topics in Microbiology and Immunology

217

189

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Section: Additional Parameters Affecting Vsv DI Interferencementioning

confidence: 83%

Origin and Replication of Defective Interfering Particles

Perrault

1981

Current Topics in Microbiology and Immunology

217

189

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“…How competitive advantages can be gained during these steps may be found in an evaluation of the RNA in VSV and in the DI particles. DI genomes contain additional complementary sequences as well as the single-base mutations (8,10,40). Because single-base mutations are in different coding regions for the L protein, it is unlikely that they are involved in interference.…”

Section: Discussionmentioning

confidence: 99%

“…This suggests that the larger genome may have more self-complementary sequences than the smaller genome. Oligonucleotide analysis indicates that both are derived from the L gene and contain sequences specific to the 5' end of the VSV RNA (10,19).…”

Section: Ns Mmentioning

confidence: 99%

Interference among defective interfering particles of vesicular stomatitis virus

Rao¹,

Huang²

1982

J Virol

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Three defective interfering (DI) particles of vesicular stomatitis virus (VSV), all derived from the same parental standard San Juan strain (Indiana serotype), were used in various combinations to infect cells together with the parental virus. The replication of their RNA genomes in the presence of other competing genomes was described by the hierarchical sequence: DI 0.52 particles > DI 0.45 particles DI-T particles > standard VSV. The advantage of one DI particle over another was not due simply to multiplicity effects nor to the irreversible occupation of linmited cellular sites. Interference, however, did correlate with a change in the ratio of plus and minus RNA templates that accumulated intracellularly and with the presence of new sequences at the 3' end of the DI genomes. DI 0.52 particles contained significantly more nucleotides at the 3' end that were complementary to those at the 5' end of its RNA than did DI-T or DI 0.45 particles. The first 45 nucleotides at the 3' ends of all of the DI RNAs were identical. VSV and its DI

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“…This conclusion is based on hybridization studies, which established that the 5' half of the DI 011 RNA is homologous to the 5' terminus of the standard genome for its entire length (33). The locations of the recombination sites within the L gene of the RNAs of DI T, T(L), and 611 are consistent with the overall size of the DI particle genomes based on hybridization data and oligonucleotide fingerprint mapping (2,7,29,35,36). In addition, the 5' terminal regions of the genomes of these DI particles are identical to the 5' terminus of VSV RNA for at least 1,167 bases (31).…”

Section: Di-t(l)mentioning

confidence: 93%

Sites of copy choice replication involved in generation of vesicular stomatitis virus defective-interfering particle RNAs

Meier¹,

Harmison²,

Keene³

et al. 1984

J Virol

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The copy choice model for the generation of defective interfering (DI) particles of vesicular stomatitis virus suggests that during replication the polymerase prematurely terminates, moves with the nascent daughter strand to another site on the same or a different template molecule, and resumes elongation of the nascent chain. We have analyzed the sites where premature termination or resumption of replication has occurred during the generation of the deletion DI particle LT, the snapback DI particle 011, and the panhandle DI particles T, T(L), and 611. The recombination sites were identified by comparing the nucleotide sequences of the relevant regions of these DI particle RNAs to those of the vesicular stomatitis virus L gene (Schubert et al., J. Virol. 51:505-514, 1984). Sequence homology was not detected between these sites, which rules out the existence of a general terminator or promoter sequence involved in copy choice replication. In several cases, however, premature termination or resumption of RNA replication may be favored by specific signal sequences. The sequences immediately before the start and at the end of the deletion in DI LT contain two hexanucleotides, ATCTGA and GATTGG, in a similar spacing. In the case of DI T and 61 1, but not of DI T(L), the end of the 5'-terminal region bears the hexanucleotide CCUCUU. This sequence is also repeated in the stem region in all three DI particle genomes. In addition, we present data that the added 3'-terminal regions of the panhandle DI particle RNAs may differ by only one base and are 46 [DI T(L) and 6111 or 45 (DI T) bases long. We suggest that each site of the vesicular stomatitis virus genome has the potential to give rise to DI particle RNAs. Specific sequences, however, may modulate this process in a quantitative way, and they favor the generation of certain types of DI particle genomes like those of the panhandle type.

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Comparison of ribonucleotide sequences from the genome of vesicular stomatitis virus and two of its defective interfering particles

Abstract: RNA genomes from standard vesicular stomatitis virus and two defective interfering (DI) particles, DI 0.33 (DI-T) and DI 0.52, were purified and digested with RNase T1. The resulting oligonucleotides were labeled at the 5' end with

Cited by 7 publications

References 26 publications

Origin and Replication of Defective Interfering Particles

Origin and Replication of Defective Interfering Particles

Interference among defective interfering particles of vesicular stomatitis virus

Sites of copy choice replication involved in generation of vesicular stomatitis virus defective-interfering particle RNAs

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