Interference among defective interfering particles of vesicular stomatitis virus

Abstract

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

Papovaviral persistent infections.

“…Thus, grossly aberrant SV40 variants frequently contain reiterations of the unique replication origin (146). For a similar reason, most DI particles of vesicular stomatitis virus (VSV) acquire the same sequence at the 3' ends of their negative-stranded genomes as at the 3' end of their plus-stranded homologs (209,224,240). This sequence is found at the 3' end of the WT plus-strand homolog, but not on the WT genome.…”

“…In some systems, interference by DI particles appears to be expressed in an all-or-none manner on a per cell basis (33, 157) rather than as a simple competition. In some instances, this might be explained by the activity of DI particles with genomes containing replicase-binding sites of much higher affinity than those of WT virus (209,224,240). Those DI particle genomes might express sufficient competition for replicase to exclude the replication of WT genomes.…”

Virus Promoters Determine Interference by Defective RNAs: Selective Amplification of Mini-RNA Vectors and Rescue from cDNA by a 3′ Copy-Back Ambisense Rabies Virus

“…Such functional constraints do not apply to DI RNAs, which are therefore rather free in promoter use. The overwhelming amount of naturally occurring VSV and paramyxovirus DI particles are 5Ј copy-back DI RNAs which contain two copies of the strong parental AGP promoter (21,22,35,37,40). While the gain of a second AGP provides a selective advantage in replication over the parental virus, and also over internal deletion DI RNAs in mixed infections (36), it is coupled with the loss of the GP and the ability to transcribe mRNAs.…”

“…Accordingly, the AGP should represent a strong replication promoter, whereas the GP should function as a weak replication promoter. This view was first supported by the structure of naturally occurring defective interfering (DI) RNAs of VSV and paramyxoviruses (36,37). Most of the DI RNAs which replicated efficiently while heavily interfering with helper virus (HV) replication were of the so-called 5Ј copy-back type, containing a copy of the strong AGP at both RNA ends.…”

Hepatitis C quasispecies adaptation in the setting of a variable fidelity polymerase

“…DIPs have also been proposed to interfere in the production of wild-type virus and modulate pathogen virulence and may themselves be potential antiviral agents. [27][28][29][30] Stumpf and Zitzmann have proposed the reciprocality of DIPs; that is, that the particles are able to replicate but are unable to cause de novo infection of new cells due to the deletion of the structural section of the genome. The associated increase in replicative ability leads to competitive exclusion of viable virions and the gradual accumulation of defective intracellular viral RNA, meaning that continuous de novo infection of new cells is essential to viral survival.…”