Covalently linked message and anti-message (genomic) RNA from a defective vesicular stomatitis virus particle

Lazzarini, Robert A.; Weber, George H.; Johnson, Leslye D.; Stamminger, Gudrun

doi:10.1016/s0022-2836(75)80042-8

Cited by 83 publications

(43 citation statements)

References 34 publications

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“…Thus it is probable that all snap-back VSV DI RNAs correspond to the structure previously proposed, i.e. a self-complementary molecule basepaired along most of its length (Lazzarini et aL 1975;Perrault, 1976). Recent evidence indicates that several DI RNAs (including a snap-back RNA) contain the same 3' and 5' termini as the parent B virion RNA (Keene, Rosenberg & Lazzarini, 1977).…”

Section: Mapping Of Snap-back Rnas By Hybridizationmentioning

confidence: 78%

“…The origin of these molecules is unclear since little is known regarding the generation of VSV DI RNAs in general. However, two main hypotheses have been suggested for the novel presence of a covalent linkage between the complementary strands: (I) a rare illegitimate event involving recombination or transcription across a replicative fork; and (2) a deleted form of a normal replicative intermediate structure (Lazzarini et al 1975;Perrault, I976). We present here evidence that snap-back RNAs are commonly found in VSV T particles and appear to conform to the same general structure.…”

Section: Introductionmentioning

confidence: 99%

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Characterization of Snap-back RNAs in Vesicular Stomatitis Defective Interfering Virus Particles

Perrault

Leavitt

1978

Journal of General Virology

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SUMMARYVSV defective interfering particles of various sizes and from several independent sources frequently contain plus and minus strand RNA. In many cases some of the complementary strands are covalently linked as snap-back molecules. Infectious particles on the other hand package little or no plus strands. Snap-back molecules from the three different sources examined so far vary in size but appear to conform to the same overall linear duplex structure with cross-links at the ends only. They each contain a base sequence which is a subset of the next larger one and appear to correspond to unique sequences in the L cistron of the genome. Possible origins for these snap-back molecules are discussed.

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Section: Mapping Of Snap-back Rnas By Hybridizationmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Characterization of Snap-back RNAs in Vesicular Stomatitis Defective Interfering Virus Particles

Perrault

Leavitt

1978

Journal of General Virology

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“…There are at least three, possibly four, classes ofDI'particle RNAs, which are structurally dissimilar. with respect to the portions of the genomic RNA retained and the amount of self-complementary sequences contained in the RNA (1)(2)(3)(4)(5).…”

mentioning

confidence: 99%

“…Under nondenaturing conditions this DI RNA exists as a hairpin duplex structure in which virtually all bases are paired (3,12). The molecular origin of this type of DI RNA has not been established yet, but the sequence near the "turnaround region" (13) suggests that the DI RNA was generated by copying both strands ofa replication fork.…”

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confidence: 99%

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Vesicular stomatitis virus defective interfering particle containing a muted internal leader RNA gene.

Keene¹,

Chien²,

Lazzarini³

1981

Proc. Natl. Acad. Sci. U.S.A.

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The RNA of a unique long defective interfering particle (DI-LT2) derived from the heat-resistant strain of vesicular stomatitis virus (VSV) contains 70 nucleotides at its 3' end that are complementary to the 5' end of the VSV RNA. Following this region of terminal complementarity, there is a precise copy of the 3' end of the nondefective VSV RNA. The sequence homology between the DI-LT2 RNA and the 3' end ofVSV RNA extends for at least 60 bases and probably for most of-the length ofthe DI-LT2RNA. The DI-LT2 particle is capable of transcription in vitro but produces only a short RNA [defective interfering (DI) particle product], which is encoded by the extreme 3' terminus of the DI. RNA. Neither leader RNA nor capped VSV mRNAs are synthesized by DI-LT2, although competent templates for these are present. These data suggest that the 3'-terminal initiation is a prerequisite of the production of, competent transcripts and that the sequence coding for leader RNA is not, by itself, sufficient for initiation. We propose a model for the origin of this DI particle, involving specific termination and resumption of replication, which is similar to that described previously for another class of DI particle RNAs. Vesicular stomatitis. virus (VSV) gives rise to defective interfering (DI) particles, which contain RNAs from which portions of the viral genome have been deleted. There are at least three, possibly four, classes ofDI'particle RNAs, which are structurally dissimilar. with respect to the portions of the genomic RNA retained and the amount of self-complementary sequences contained in the RNA (1-5).The first and major class of defective particle RNAs has retained the 5' portion of the VSV genome and contains RNA molecules ofvarious sizes (0.1-0.5 of the VSV RNA). These DI particle RNAs have complementary terminal base sequences, a property not shared by the VSV RNA. Both hybridization studies and direct. sequence analysis have shown that the DI RNAs contain a 46-to 48-nucleotide sequence at their 3' termini that is not found on the parental viral genome (6-10). Recently, we have analyzed several DI RNAs of this class and hypothesized that a specific internalpolymerase recognition site located 4348 nucleotides from the 5' end of VSV RNA was involved in the origin of the terminal complementarity (11). This hypothesis is consistent with the model ofLeppert et al. (9), which predicts that the complementary ends of the DI particle RNAs result from an aberration of viral replication-the polymerase and nascent daughter strand detach from the nucleocapsid template. and the polymerase resumes synthesis using its own daughter strand as a template, thereby generating the complementary terminus.A second class of DI particle contains an RNA that.is homologous to the 5' portion of-the VSV genome and is covalently linked to the complement of this RNA. Under nondenaturing conditions this DI RNA exists as a hairpin duplex structure in which virtually all bases are paired (3,12). The molecular origin of this type of DI RNA has ...

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Persistent measles virus infection in vitro and in man

Viola

Scott

Duffy

1978

Arthritis & Rheumatism

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The characteristics of cell lines persistently infected with measles virus are described. Molecular mechanisms for measles virus‐persistence in vitro as well as in human disease include defective interfering particles, mutant virus strains, proviral DNA, and nonpermissive cell types. The role of measles virus in subacute sclerosing panencephalitis and evidence for measles virus infection in multiple sclerosis, Paget's disease, and systemic lupus erythematosus are discussed.

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Covalently linked message and anti-message (genomic) RNA from a defective vesicular stomatitis virus particle

Cited by 83 publications

References 34 publications

Characterization of Snap-back RNAs in Vesicular Stomatitis Defective Interfering Virus Particles

Characterization of Snap-back RNAs in Vesicular Stomatitis Defective Interfering Virus Particles

Vesicular stomatitis virus defective interfering particle containing a muted internal leader RNA gene.

Persistent measles virus infection in vitro and in man

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