Synthesis of a small RNA in cells coinfected by standard and defective interfering particles of vesicular stomatitis virus.

Rao, Donald D.; Huang, Alice S.

doi:10.1073/pnas.76.8.3742

Cited by 16 publications

(15 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Besides the viral mRNA, two small transcripts can be synthesized, the positive-stranded leader (leRNA) and negativestranded trailer (trRNA) (150,151,231). They are transcribed from the genome 3Ј end, which contains the transcription and genomic promoters, and from the antigenome 3Ј end, encompassing the antigenomic promoter, respectively (54,105).…”

Section: Virus Replication Cyclementioning

confidence: 99%

Interplay between Innate Immunity and Negative-Strand RNA Viruses: towards a Rational Model

Gerlier

Lyles

2011

Microbiol Mol Biol Rev

View full text Add to dashboard Cite

SUMMARY The discovery of a new class of cytosolic receptors recognizing viral RNA, called the RIG-like receptors (RLRs), has revolutionized our understanding of the interplay between viruses and host cells. A tremendous amount of work has been accumulating to decipher the RNA moieties required for an RLR agonist, the signal transduction pathway leading to activation of the innate immunity orchestrated by type I interferon (IFN), the cellular and viral regulators of this pathway, and the viral inhibitors of the innate immune response. Previous reviews have focused on the RLR signaling pathway and on the negative regulation of the interferon response by viral proteins. The focus of this review is to put this knowledge in the context of the virus replication cycle within a cell. Likewise, there has been an expansion of knowledge about the role of innate immunity in the pathophysiology of viral infection. As a consequence, some discrepancies have arisen between the current models of cell-intrinsic innate immunity and current knowledge of virus biology. This holds particularly true for the nonsegmented negative-strand viruses ( Mononegavirales ), which paradoxically have been largely used to build presently available models. The aim of this review is to bridge the gap between the virology and innate immunity to favor the rational building of a relevant model(s) describing the interplay between Mononegavirales and the innate immune system.

show abstract

Section: Virus Replication Cyclementioning

confidence: 99%

Interplay between Innate Immunity and Negative-Strand RNA Viruses: towards a Rational Model

Gerlier

Lyles

2011

Microbiol Mol Biol Rev

View full text Add to dashboard Cite

show abstract

“…Recently a small RNA, lacking polyadenylate [poly(A)] at the 3' end and containing (p)ppAp at the 5' end, was found by direct radiolabeling with 32P of cells coinfected with standard VSV and defective interfering (DI) particles (28). Identical small RNAs of 45 to 47 nucleotides are made in vitro by DI particles in a polymerase assay (7,29,30).…”

mentioning

confidence: 99%

RNA synthesis of vesicular stomatitis virus. X. Transcription and replication by defective interfering particles

Rao¹,

Huang²

1980

J Virol

Self Cite

View full text Add to dashboard Cite

In cells coinfected by standard vesicular stomatitis virus (VSV) and defective interfering (DI) T particles, small RNA consisting of 46 nucleotides was synthesized in molar excess over other VSV-specific RNAs. Although its rate of synthesis increased over time, small RNA accumulated linearly, suggesting that the molecule is unstable. In contrast, replication of the genome RNA of DI T particles was relatively constant after 3 h of infection, resulting in the intracellular accumulation of stable genomic and antigenomic RNA of DI T particles. Coinfection of cells with DI T particles and selected temperature-sensitive mutants from all five complementation groups of VSV indicated that the replication of DI genomes was controlled separately from the synthesis of small RNA. Also, when viral RNA replication was inhibited by cycloheximide, small RNA continued to be synthesized as long as there were enough templates present. These results indicate that small RNA is synthesized by the enzyme(s) involved in VSV transcription and that its dependence on RNA replication is due to the requirement for template amplification.

show abstract

“…some trapped RNA. Agarose gel patterns of ted from the RNA obtained from cells infected with only d in various standard VSV have been published (19,34,35). ird VSV to When cells were triply infected with any two r any one of of the DI particles and standard VSV, 40S RNA re effective synthesis was still inhibited, but there were e. This was varying degrees of replication of the genomes of t of intracel-DI particles.…”

Section: Resultsmentioning

confidence: 99%

“…RNA was harvested at 6 h after infection and separated on a 1.5% agarose gel. (a) DI 0.52 particles at 0 h, 32P at 1 to 6 h; (b) DI 0.52 particles at 0.5 h, 32P at 1.5 to 6 h; (c) cycloheximide at 0 to 1 h, DI 0.52 particles at 0.5 h, 32p at 1.5 to 6 h; (d) DI 0.52 particles at 1 h, 32P at 2 to 6 h; (e) cycloheximide at 0 to 1.5 h, DI 0.52 particles at 1 h, 32p at 2 to 6 h. (34,35). Sma hybridized against unlabeled virio pared from standard VSV or DI well as against total unlabeled intra< from singly or coinfected cells.…”

Section: Ns Mmentioning

confidence: 94%

“…Cloned and sucrose gradient-purified standard VSV of the Indiana serotype (San Juan strain) and three size classes of DI particles derived from this same standard strain were used. According to a recent agreement (36), the three DI particles are designated: VSI ts+ SJ DI-T/DI 0.33 (5') (15,19); VSI ts+ SJ DI 0.52 (5') (19,34); and VSI ts+ SJ DI LT/DI 0.45 (5') (5). DI 0.45 was kindly supplied by Sue Emerson (University of Virginia, Charlottesville).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Interference among defective interfering particles of vesicular stomatitis virus

Rao¹,

Huang²

1982

J Virol

Self Cite

View full text Add to dashboard Cite

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

show abstract

Synthesis of a small RNA in cells coinfected by standard and defective interfering particles of vesicular stomatitis virus.

Cited by 16 publications

References 26 publications

Interplay between Innate Immunity and Negative-Strand RNA Viruses: towards a Rational Model

Interplay between Innate Immunity and Negative-Strand RNA Viruses: towards a Rational Model

RNA synthesis of vesicular stomatitis virus. X. Transcription and replication by defective interfering particles

Interference among defective interfering particles of vesicular stomatitis virus

Contact Info

Product

Resources

About