Conditional lethal mutants of vesicular stomatitis virus IV. RNA species detected in nonpermissive cells infected with host-restricted mutants

Morrongiello, Mary Pat; Simpson, Robert W.

doi:10.1016/0042-6822(79)90253-8

Cited by 10 publications

(2 citation statements)

References 33 publications

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“…These mutants grow well at 35°C in permissive baby hamster kidney cells or chicken embryo fibroblasts but are severely restricted in many human cell lines, including HEp-2 cells (11). Studies by Simpson and co-workers (10,12) 24 hr at 350C or 370C, respectively. WT VSV grown at either 370C or 350C gave identical in vitro methylation patterns.…”

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confidence: 99%

Host range mutants of vesicular stomatitis virus defective in in vitro RNA methylation.

Horikami¹,

Moyer²

1982

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

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The viral RNA polymerase of detergent-treated vesicular stomatitis virus normally synthesizes viral mRNAs in vitro that are both guanylylated and methylated to give 5'-terminal 7mGpppAm caps. We have characterized a virus host range mutant, hr 1, that is totally defective in vitro in the methylation of mRNA, although full-length polyadenylylated mRNAs with 5' termini of the form GpppA are synthesized in normal yields. A second mutant, hr 8, is partially defective in methylation and synthesizes mRNAs in vitro with primarily GpppA and some GpppAm 5' termini. When used for in vitro translation, the unmethylated hr 1 mutant mRNA shows, as expected, reduced synthesis of viral proteins. These data provide direct evidence that the vesicular stomatitis virus-associated methyltransferase activities are virus encoded.

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confidence: 99%

Host range mutants of vesicular stomatitis virus defective in in vitro RNA methylation.

Horikami¹,

Moyer²

1982

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

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“…Genetic and biochemical studies have established that the replication of vesicular stomatitis virus (VSV) in permissive cells requires unidentified host factors. Host range or host restricted (hr) mutants of VSV previously isolated in this laboratory have been shown to involve impaired virusspecific RNA synthesis in nonpermissive cells and the requirement for multiple host factors based on positive complementation reactions between certain combinations of these mutants (Simpson et d, 1979;Morrongiello and Simpson, 1979). Two of these hr mutants were recently shown to involve defective in vitro methylation of viral mRNA species (Horikami and Moyer,1 Author to whom requests for reprints should be addressed.…”

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confidence: 99%

Reversible restriction of vesicular stomatitis virus in permissive cells treated with inhibitors of prostaglandin biosynthesis

Mukherjee

Simpson

1984

Virology

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Indomethacin, a potent nonsteroidal inhibitor of prostaglandin synthetase (cyclooxygenase) reduced yields of infectious vesicular stomatitis virus in HEp-2 cells more than 99% if added to cultures at levels of 10(-3)M either before or after infection. Other permissive cell lines differed according to the treatment period and drug level required for restricting productive infections. The inhibitory effect of indomethacin was progressively reduced if infection of cells was delayed for increasing times after drug removal. Strong inhibition of viral replication also occurred in cells treated with the cyclooxygenase antagonists naproxen, phenylbutazone, and oxyphenylbutazone whereas phenacetin, which does not block cyclooxygenase function, was inactive. Enhanced viral replication occurred in indomethacin-treated HEp-2 cultures when these cells were subsequently exposed to such substances as prostaglandin E1, cyclic AMP, or insulin. Conversely, indomethacin-treated cells remained restrictive for VSV if they were subsequently exposed to metabolic inhibitors of functional DNA (actinomycin D or mitomycin C), messenger RNA synthesis (alpha-amanitin), or protein synthesis (cycloheximide) at concentrations that normally do not compromise viral replication. Pretreatment of HEp-2 cells with mitomycin C markedly shifted the dose response for indomethacin-mediated inhibition of VSV from a 90% inhibitory dose of about 10(-4)M to one of 10(-9)M or lower. These findings suggest that preexisting host factors essential for replication of VSV, although rendered nonfunctional by the drug indomethacin, can be replenished unless their synthesis is blocked by various classes of metabolic inhibitors.

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Rhabdovirus Genetics

Pringle¹

1987

The Rhabdoviruses

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There are five families of RNA viruses in which the negative strand is sequestered in the extracellular virion. Viruses of two of these families, the Rhabdoviridae and the Paramyxoviridae, have unitary linear genomes, whereas viruses of the other three families, Arenaviridae, Bunyaviridae, and Orthomyxoviridae, have segmented genomes comprising, respectively, two, three, and seven or eight subunits. The informational macromolecules that comprise the genomes of rhabdoviruses and paramyxoviruses are among the largest functional RNA molecules and are exceeded in size only by those of the plus-strand coronaviruses. Reanney (1982Reanney ( , 1984 has calculated that the upper size limit for any RNA virus genome cannot be much in excess of 17,600 nucleotides (mol. wt. =5.7 x 10 6 ) as a consequence of the low copying fidelity of RNA polymerases. The segmentation of the genomes of the other negative-strand viruses may be a consequence of such constraints on molecular size or a device for decoupling the transcription of !ndividual genes. Whatever the reason, the genetic properties of the segmented-genome viruses differ substantially from those of the unsegmented-genome viruses, because variation in the former is generated by reassortment of genome subunits as well as by mutation. Mutation is the sole mechanism of variation in unsegmented-genome viruses, since the intramolecular recombination observed with positive-

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Conditional lethal mutants of vesicular stomatitis virus IV. RNA species detected in nonpermissive cells infected with host-restricted mutants

Cited by 10 publications

References 33 publications

Host range mutants of vesicular stomatitis virus defective in in vitro RNA methylation.

Host range mutants of vesicular stomatitis virus defective in in vitro RNA methylation.

Reversible restriction of vesicular stomatitis virus in permissive cells treated with inhibitors of prostaglandin biosynthesis

Rhabdovirus Genetics

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