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PubMed2006

Yeast viral killer toxins: lethality and self-protection.

Since the discovery of toxin-secreting killer yeasts more than 40 years ago, research into this phenomenon has provided insights into eukaryotic cell biology and virus-host-cell interactions. This review focuses on the most recent advances in our understanding of the basic biology of virus-carrying killer yeasts, in particular the toxin-encoding killer viruses, and the intracellular processing, maturation and toxicity of the viral protein toxins. The strategy of using eukaryotic viral toxins to effectively penetrate and eventually kill a eukaryotic target cell will be discussed, and the cellular mechanisms of self-defence and protective immunity will also be addressed.

Apoptosis↗
PubMed1985

Interferon induction by viruses. XII. Inhibition of protein synthesis renders aged chick embryo cells refractory to interferon induction.

The initial stages of interferon induction in mouse L cells do not require protein synthesis; all steps in the induction process up to and including the transcription of interferon mRNA occurred in the presence of inhibitors of protein synthesis. In contrast, interferon induction in primary chick embryo cells aged in vitro does require a reaction that depends upon protein synthesis, unique in that it is not required for virus replication or the action of interferon.

Animals↗
PubMed2000

Essential and dispensable virus-encoded replication elements revealed by efforts To develop hypoviruses as gene expression vectors.

We have investigated whether hypoviruses, viral agents responsible for virulence attenuation (hypovirulence) of the chestnut blight fungus Cryphonectria parasitica, could serve as gene expression vectors. The infectious cDNA clone of the prototypic hypovirus CHV1-EP713 was modified to generate 20 different vector candidates. Although transient expression was achieved for a subset of vectors that contained the green fluorescent protein gene from Aequorea victoria, long-term expression (past day 8) was not observed for any vector construct. Analysis of viral RNAs recovered from transfected fungal colonies revealed that the foreign genes were readily deleted from the replicating virus, although small portions of foreign sequences were retained by some vectors after months of replication. However, the results of vector viability and progeny characterization provided unexpected new insights into essential and dispensable elements of hypovirus replication. The N-terminal portion (codons 1 to 24) of the 5'-proximal open reading frame (ORF), ORF A, was found to be required for virus replication, while the remaining 598 codons of this ORF were completely dispensable. Substantial alterations were tolerated in the pentanucleotide UAAUG that contains the ORF A termination codon and the overlapping putative initiation codon of the second of the two hypovirus ORFs, ORF B. Replication competence was maintained following either a frameshift mutation that caused a two-codon extension of ORF A or a modification that produced a single-ORF genomic organization. These results are discussed in terms of determinants of hypovirus replication, the potential utility of hypoviruses as gene expression vectors, and possible mechanisms by which hypoviruses recognize and delete foreign sequences.

Amino Acid Sequence↗
PubMed2006

Innate immune recognition of viral infection.

Induction of the antiviral innate immune response depends on recognition of viral components by host pattern-recognition receptors. Members of the Toll-like receptor family have emerged as key sensors that recognize viral components such as nucleic acids. Toll-like receptor signaling results in the production of type I interferon and inflammatory cytokines and leads to dendritic cell maturation and establishment of antiviral immunity. Cells also express cytoplasmic RNA helicases that function as alternative pattern-recognition receptors through recognition of double-stranded RNA produced during virus replication. These two classes of pattern-recognition receptor molecules are expressed in different intracellular compartments and induce type I interferon responses via distinct signaling pathways.

Adaptor Proteins, Signal Transducing↗
PubMed1997

Nucleotide sequence comparison of the segments S10 of the nine African horsesickness virus serotypes.

Segments 10 (S10) of the double-stranded RNA (ds RNA) genomes from African horsesickness virus (AHSV) serotypes 2, 4, 5, 6 and 7 were cloned and sequenced. Direct sequencing of previously reverse transcribed amplified (RT)-PCR segments S10 was also performed. Nucleotide sequences of two strains (the virulent Moroccan strain and a vaccine strain) of the same serotype (4) were determined. Sequences of the viral serotypes were analysed and compared to each other. Two in-phase ATG codons were conserved in the S10 of AHSV-2, AHSV-4, AHSV-5, AHSV-6 and AHSV-7 and were considered candidate translation initiation codons of NS3 and NS3A respectively. A close relationship between serotypes 4, 5 and 9 and between serotypes 3 and 7 were described. Closer relationships of serotype 2 to the 1 and 8 group on one hand and of serotype 6 to the 4, 5 and 9 group on the other hand were observed.

African Horse Sickness Virus↗
PubMed1979

Peptide map comparison of the proteins of infectious bursal disease virus.

The genome of infectious bursal disease virus consists of two segments of double-stranded RNA of 2.5 X 10(6) and 2.2 X 10(6) molecular weight. Polyacrylamide gel electrophoresis of purified virus resolved four structural polypeptides: VP-1 (90,000), VP-2 (41,000), VP-3 (35,000), and VP-4 (28,000). Peptide map comparisons of radioiodinated virion proteins indicated no precursor-product relationship between them. The possible relationship between the size of the virus genome and the number and sizes of different viral proteins is discussed.

Genes, Viral↗
PubMed1984

Genome structure and expression of a defective interfering mutant of the killer virus of yeast.

A large internal deletion in M1 double-stranded (ds) RNA from the killer virus of Saccharomyces cerevisiae generates a suppressive (S3) dsRNA molecule. Strains which harbor S3 dsRNA are defective in toxin production and immunity to the toxin. The biochemical defect in expression has been investigated and is apparently due to truncation of the protoxin polypeptide translation reading frame on S3 dsRNA. Transcription in vivo, and in isolated virions in vitro, results in the synthesis of a full-length positive polarity messenger RNA, denoted s. The s transcript contains no long poly(A) tracts as determined by its lack of affinity for oligo(dT)-cellulose, and as inferred by sequence analysis of approximately 87% of the S3 dsRNA genome. These data support a model for template coding of polyadenylate in transcripts derived from the wild-type M1 dsRNA. The orientation of the sequences conserved on S3 dsRNA with respect to M1 dsRNA has been determined. Some of the conserved sequences are likely to be required for the maintenance and replication of these viral dsRNA genomes in S. cerevisiae.

Amino Acid Sequence↗
PubMed2000

Influenza A virus NS1 protein prevents activation of NF-kappaB and induction of alpha/beta interferon.

The alpha/beta interferon (IFN-alpha/beta) system represents one of the first lines of defense against virus infections. As a result, most viruses encode IFN antagonistic factors which enhance viral replication in their hosts. We have previously shown that a recombinant influenza A virus lacking the NS1 gene (delNS1) only replicates efficiently in IFN-alpha/beta-deficient systems. Consistent with this observation, we found that infection of tissue culture cells with delNS1 virus, but not with wild-type influenza A virus, induced high levels of mRNA synthesis from IFN-alpha/beta genes, including IFN-beta. It is known that transactivation of the IFN-beta promoter depends on NF-kappaB and several other transcription factors. Interestingly, cells infected with delNS1 virus showed high levels of NF-kappaB activation compared with those infected with wild-type virus. Expression of dominant-negative inhibitors of the NF-kappaB pathway during delNS1 virus infection prevented the transactivation of the IFN-beta promoter, demonstrating a functional link between NF-kappaB activation and IFN-alpha/beta synthesis in delNS1 virus-infected cells. Moreover, expression of the NS1 protein prevented virus- and/or double-stranded RNA (dsRNA)-mediated activation of the NF-kappaB pathway and of IFN-beta synthesis. This inhibitory property of the NS1 protein of influenza A virus was dependent on its ability to bind dsRNA, supporting a model in which binding of NS1 to dsRNA generated during influenza virus infection prevents the activation of the IFN system. NS1-mediated inhibition of the NF-kappaB pathway may thus play a key role in the pathogenesis of influenza A virus.

Animals↗
PubMed1993

Virus inactivation by copper or iron ions alone and in the presence of peroxide.

Cupric and ferric ions were able to inactivate five enveloped or nonenveloped, single- or double-stranded DNA or RNA viruses. The virucidal effect of these metals was enhanced by the addition of peroxide, particularly for copper(II). Under the conditions of our test, mixtures of copper(II) ions and peroxide were more efficient than glutaraldehyde in inactivating phi X174, T7, phi 6, Junin, and herpes simplex viruses. The substances described here should be able to inactivate most, if not all, viruses that have been found contaminating medical devices.

Copper↗
PubMed1984

Saccharomyces cerevisiae killer virus transcripts contain template-coded polyadenylate tracts.

The M double-stranded RNA component of type 1 killer strains of the yeast Saccharomyces cerevisiae contains an internal 200-base pair adenine- and uracil-rich region. The plus strands of this viral genomic RNA contain an internal adenine-rich region which allows these strands to bind to polyuridylate-Sepharose as tightly as do polyadenylated RNAs with 3'-terminal polyadenylated tracts of 70 to 100 residues. Internal template coding of an adenine-rich tract in positive polarity in vivo and in vitro transcripts of M double-stranded RNA may serve as an alternate method of transcript polyadenylation. The 3'-terminal residue of the in vitro m transcript is a non-template-encoded purine residue. The 5' terminus of this transcript is involved in a stem-and-loop structure which includes an AUG initiation codon, along with potential 18S and 5.8S rRNA binding sites. Except for the 3'-terminal residue, transcription in in vitro shows complete fidelity.

Base Sequence↗
PubMed1973

Increased toxicity of double-stranded ribonucleic acid in virus-infected animals.

Virus-infected mice were significantly more susceptible to the toxic effects of double-stranded ribonucleic acid (RNA) than uninfected mice. A dramatic increase in mortality was observed after injection of either synthetic (polyriboinosinic.polyribocytidylic acid) or natural (mycophage) double-stranded RNA in mice infected with Newcastle disease virus (NDV) or vesicular stomatitis virus (VSV). With the exception of endotoxin, interferon inducers other than double-stranded RNA, such as tilorone-hydrochloride and chlorite-oxidized oxyamylose, did not show this increased toxicity in virus-infected animals. The increased susceptibility of virus-infected animals to the toxic effects of double-stranded RNA appears to be related to the levels of interferon induced by the virus infection, either systemically, in the blood stream (after inoculation of NDV), or locally, in the brain (after infection with VSV).

Animals↗
PubMed2006

Four plant Dicers mediate viral small RNA biogenesis and DNA virus induced silencing.

Like other eukaryotes, plants use DICER-LIKE (DCL) proteins as the central enzymes of RNA silencing, which regulates gene expression and mediates defense against viruses. But why do plants like Arabidopsis express four DCLs, a diversity unmatched by other kingdoms? Here we show that two nuclear DNA viruses (geminivirus CaLCuV and pararetrovirus CaMV) and a cytoplasmic RNA tobamovirus ORMV are differentially targeted by subsets of DCLs. DNA virus-derived small interfering RNAs (siRNAs) of specific size classes (21, 22 and 24 nt) are produced by all four DCLs, including DCL1, known to process microRNA precursors. Specifically, DCL1 generates 21 nt siRNAs from the CaMV leader region. In contrast, RNA virus infection is mainly affected by DCL4. While the four DCLs are partially redundant for CaLCuV-induced mRNA degradation, DCL4 in conjunction with RDR6 and HEN1 specifically facilitates extensive virus-induced silencing in new growth. Additionally, we show that CaMV infection impairs processing of endogenous RDR6-derived double-stranded RNA, while ORMV prevents HEN1-mediated methylation of small RNA duplexes, suggesting two novel viral strategies of silencing suppression. Our work highlights the complexity of virus interaction with host silencing pathways and suggests that DCL multiplicity helps mediate plant responses to diverse viral infections.

Arabidopsis↗
PubMed1991

Encephalomyocarditis virus RNA polymerase preparations, with and without RNA helicase activity.

RNA template- and primer-dependent preparations of RNA polymerase were purified from encephalomyocarditis virus-infected Krebs-2 cells, using a three-step chromatographic procedure. The RNA duplex-unwinding activity of these preparations was investigated by two assays, using a partially double-stranded RNA template (encephalomyocarditis virus RNA annealed with a long segment of antisense transcript). Less purified preparations of the polymerase appeared to be able to efficiently displace, in an ATP-dependent and RNA elongation-dependent reaction, the antisense segment from the template. However, upon a more extensive purification, the unwinding activity of the RNA polymerase preparations was lost.

Chromatography↗
PubMed1996

Mutational analysis of the vaccinia virus E3 protein defines amino acid residues involved in E3 binding to double-stranded RNA.

Alanine-substitution mutations were targeted to 14 amino acid residues within the double-stranded (ds) RNA binding motif (dsRBM) of the vaccinia virus E3 protein. Substitutions at six positions--Glu-124, Phe-135, Phe-148, Lys-167, Arg-168, and Lys-171--caused significant reductions in dsRNA binding. These six residues are conserved in the two dsRBMs for which structural information is available (Escherichia coli RNase III and Drosophila melanogaster staufen) and in many other members of the dsRBM protein family. Residues we show to be important for dsRNA binding by vaccinia virus E3 map to the same face of the dsRBM structure and are thus likely to compose part of the RNA binding site.

Amino Acid Sequence↗
PubMed2005

Differential induction of antiviral effects against West Nile virus in primary mouse macrophages derived from flavivirus-susceptible and congenic resistant mice by alpha/beta interferon and poly(I-C).

A cell model of primary macrophages isolated from the peritoneal cavity of flavivirus-susceptible and congenic resistant mice has been used to study the extent and kinetics of antiviral effects against West Nile virus upon priming with alpha/beta interferon (IFN-alpha/beta) or poly(I-C) (pIC). The pattern of flavivirus resistance expressed after priming of cells in this model was in good agreement with the pattern of flavivirus resistance described in the brains of the corresponding mouse strains. While priming with either IFN-alpha/beta or pIC completely blocked flavivirus replication in macrophages from resistant mice, it only transiently reduced flavivirus replication in macrophages from susceptible mice. It was only the combined pretreatment with IFN-alpha/beta and pIC that elicited strong antiviral responses that completely prevented flavivirus replication in macrophages from susceptible mice. Primary macrophages isolated from the blood of healthy human donors expressed a similar need for double-stranded RNA (dsRNA) cofactor in developing efficient antiviral responses against West Nile virus. These findings reveal that the inefficient IFN-alpha/beta-induced antiviral effects against flaviviruses in cells from susceptible hosts could be successfully complemented by an external dsRNA factor leading to the complete eradication of the virus. This treatment appears to compensate for the lack of an inborn resistance mechanism in cells from the susceptible host. Furthermore, it may also provide useful clues for the prevention and treatment of flavivirus infections.

Animals↗
PubMed2005

Three unrelated viruses occur in a single isolate of Gremmeniella abietina var. abietina type A.

Five enclosed double-stranded RNA (dsRNA) bands in electrophoresis, probably of viral origin, were found from a single isolate (SurS4) of Gremmeniella abietina var. abietina type A. Analysis of the dsRNAs revealed that they represented three different viruses, named as Gremmeniella abietina mitochondrial RNA virus S2 (GaMRV-S2), Gremmeniella abietina RNA virus MS2 (GaRV-MS2) and Gremmeniella abietina RNA virus L2 (GaRV-L2). The genome of GaMRV-S2 was 2587 base pairs (bp) long and had a very low GC content (31%). Sequence variations occurred at both ends. The genome coded for a putative RNA-dependent RNA polymerase (RdRp) under a mitochondrial translation code. The GaRV-MS2 genome was composed of three dsRNA molecules (1781 bp, 1586 bp and 1186 bp). They coded for a putative RdRp, a coat protein (CP) and a protein with an unknown function, respectively. The GaRV-L2 genome was 5129 bp long and contained two ORFs. The 5'-proximal ORF coded for a putative CP, whereas the 3'-proximal ORF encoded for a putative RdRp. The buoyant density of GaRV-MS2 and GaRV-L2 were 1.37 and 1.42 g/ml, respectively. GaMRV-S2, GaRV-MS2 and GaRV-L2 were closely related to the previously described viruses GaMRV-S1, GaRV-MS1 and GaRV-L1, respectively, and are putative members of the genera Mitovirus, Partitivirus and Totivirus, respectively. This is the first report on the occurrence of viruses of all these different genera in a single fungal isolate.

Amino Acid Sequence↗
PubMed2002

The Zygosaccharomyces bailii antifungal virus toxin zygocin: cloning and expression in a heterologous fungal host.

Zygocin, a monomeric protein toxin secreted by a virus-infected killer strain of the osmotolerant spoilage yeast Zygosaccharomyces bailii, kills a broad spectrum of human and phytopathogenic yeasts and filamentous fungi by disrupting cytoplasmic membrane function. The toxin is encoded by a double-stranded (ds)RNA killer virus (ZbV-M, for Z. bailii virus M) that stably persists within the yeast cell cytosol. In this study, the protein toxin was purified, its N-terminal amino acid sequence was determined, and a full-length cDNA copy of the 2.1 kb viral dsRNA genome was cloned and successfully expressed in a heterologous fungal system. Sequence analysis as well as zygocin expression in Schizosaccharomyces pombe indicated that the toxin is in vivo expressed as a 238-amino-acid preprotoxin precursor (pptox) consisting of a hydrophobic N-terminal secretion signal, followed by a potentially N-glycosylated pro-region and terminating in a classical Kex2p endopeptidase cleavage site that generates the N-terminus of the mature and biologically active protein toxin in a late Golgi compartment. Matrix-assisted laser desorption mass spectrometry further indicated that the secreted toxin is a monomeric 10.4 kDa protein lacking detectable post-translational modifications. Furthermore, we present additional evidence that in contrast with other viral antifungal toxins, zygocin immunity is not mediated by the toxin precursor itself and, therefore, heterologous pptox expression in a zygocin-sensitive host results in a suicidal phenotype. Final sequence comparisons emphasize the conserved pattern of functional elements present in dsRNA killer viruses that naturally infect phylogenetically distant hosts (Saccharomyces cerevisiae and Z. bailii) and reinforce models for the sequence elements that are in vivo required for viral RNA packaging and replication.

Amino Acid Sequence↗