Cucumber vein yellowing virus isolate-specific expression of symptoms and viral RNA accumulation in susceptible and resistant cucumber cultivars

2013 ◽  
Vol 43 ◽  
pp. 141-145 ◽  
Author(s):  
L. Galipienso ◽  
D. Janssen ◽  
L. Rubio ◽  
J. Aramburu ◽  
L. Velasco
Keyword(s):  
Virus Isolate ◽  
Viral Rna ◽  
Specific Expression ◽  
Rna Accumulation ◽  
Yellowing Virus

scholarly journals Contribution of Protein p40 to Hypovirus-Mediated Modulation of Fungal Host Phenotype and Viral RNA Accumulation

2002 ◽  
Vol 76 (15) ◽  
pp. 7747-7759 ◽  
Author(s):  
Nobuhiro Suzuki ◽  
Donald L. Nuss
Keyword(s):  
Function Analysis ◽  
Viral Rna ◽  
Laccase Production ◽  
Terminal Portion ◽  
Gain Of Function ◽  
Sequence Element ◽  
Fungal Virulence ◽  
Fungal Strains ◽  
Accessory Function ◽  
Rna Accumulation

ABSTRACT The papain-like protease p29, derived from the N-terminal portion of the hypovirus CHV1-EP713-encoded open reading frame (ORF) A polyprotein, p69, was previously shown to contribute to reduced pigmentation and sporulation by the infected host, the chestnut blight fungus Cryphonectria parasitica, while being dispensable for virus replication and attenuation of fungal virulence (hypovirulence). We now report that deletion of the C-terminal portion of p69, which encodes the highly basic protein p40, resulted in replication-competent mutant viruses that were, however, significantly reduced in RNA accumulation. While the Δp40 mutants retained the ability to confer hypovirulence, Δp40-infected fungal strains produced more asexual spores than strains infected with either wild-type CHV1-EP713 or a Δp29 mutant virus. As observed for Δp29-infected colonies, pigment production was significantly increased in Δp40-infected fungal strains relative to that in CHV1-EP713-infected strains. Virus-mediated suppression of laccase production was not affected by p40 deletion. A gain-of-function analysis was employed to map the p40 symptom determinant to the N-terminal domain, encompassing p69 amino acid residues Thr(288) to Arg(312). Evidence that the gain of function was due to the encoded protein rather than the corresponding RNA sequence element was provided by introducing frameshift mutations on either side of the activity determinant domain. Moreover, restoration of symptoms correlated with increased accumulation of viral RNA. These results suggest that p40 indirectly contributes to virus-mediated suppression of fungal pigmentation and conidiation by providing an accessory function in hypovirus RNA amplification. A possible role for p40 in facilitating ORF B expression and the relationship between hypovirus RNA accumulation and symptom expression are discussed.

scholarly journals A Moonlighting microRNA: Mechanism(s) of miR-122-Mediated Viral RNA Accumulation

Proceedings ◽  
2020 ◽  
Vol 50 (1) ◽  
pp. 131
Author(s):  
Jasmin Chahal ◽  
Luca FR Gebert ◽  
Hin Hark Gan ◽  
Kristin C Gunsalus ◽  
Ian J MacRae ◽  
...  
Keyword(s):  
Cell Culture ◽  
Viral Genome ◽  
Rna Virus ◽  
Internal Ribosomal Entry Site ◽  
Viral Rna ◽  
Antiviral Resistance ◽  
Hcv Rna ◽  
Entry Site ◽  
Rna Chaperone ◽  
Rna Accumulation

Hepatitis C virus (HCV) is a positive-sense RNA virus that interacts with a human-liver-specific microRNA, termed miR-122. miR-122 binds to two sites in the 5' untranslated region (UTR) of the viral genome, and this interaction promotes HCV RNA accumulation. This interaction is important for viral RNA accumulation in cell culture, and miR-122 inhibitors have been demonstrated to be efficacious in reducing HCV titers in chronic HCV-infected patients. However, the precise mechanism(s) of miR-122-mediated viral RNA accumulation have remained elusive. We have used biophysical analysis and assays for viral replication in cell culture to understand the interactions between the human Argonaute 2 (hAgo2):miR-122 complex and the HCV genome. In addition, we have analyzed several resistance-associated variants which were isolated from patients who underwent miR-122 inhibitor-based therapy in order to shed light on novel mechanisms of antiviral resistance. Our results provide a new model for miR-122:HCV RNA interactions and demonstrate that miR-122 plays at least three roles in the HCV life cycle: (1) miR-122 acts as an RNA chaperone to suppress an energetically favorable secondary structure and allows the viral internal ribosomal entry site (IRES) to form; (2) miR-122 binding to the 5' terminus protects the genome from the activity of cellular pyrophosphatases (DOM3Z and DUSP11) and subsequent exonuclease-mediated decay; and (3) the Argonaute (Ago) protein at Site 2 makes direct contact with the HCV IRES, enhancing viral translation. In addition, analyses of several resistance-associated variants that were isolated from patients that underwent miR-122 inhibitor-based therapy suggests that mutations in the 5' terminus alter the structure of the 5' UTR in a manner that promotes RNA chaperone activity or viral genome stability, even in the absence of miR-122. Taken together, these findings provide insight into the mechanism(s) of miR-122-mediated viral RNA accumulation and suggest new mechanisms of antiviral resistance which are mediated by changes in RNA structure.

scholarly journals Peanut Clump Virus RNA-1-Encoded P15 Regulates Viral RNA Accumulation but Is Not Abundant at Viral RNA Replication Sites

2001 ◽  
Vol 75 (4) ◽  
pp. 1941-1948 ◽  
Author(s):  
Patrice Dunoyer ◽  
Etienne Herzog ◽  
Odile Hemmer ◽  
Christophe Ritzenthaler ◽  
Christiane Fritsch
Keyword(s):  
Laser Scanning ◽  
Fluorescent Protein ◽  
Laser Scanning Confocal Microscopy ◽  
Viral Rna ◽  
Epifluorescence Microscopy ◽  
Scanning Confocal Microscopy ◽  
Virus Rna ◽  
Green Fluorescent ◽  
Rna Accumulation

ABSTRACT RNA-1 of peanut clump pecluvirus (PCV) encodes N-terminally overlapping proteins which contain helicase-like (P131) and polymerase-like (P191) domains and is able to replicate in the absence of RNA-2 in protoplasts of tobacco BY-2 cells. RNA-1 also encodes P15, which is expressed via a subgenomic RNA. To investigate the role of P15, we analyzed RNA accumulation in tobacco BY-2 protoplasts inoculated with RNA-1 containing mutations in P15. For all the mutants, the amount of progeny RNA-1 produced was significantly lower than that obtained for wild-type RNA-1. If RNA-2 was included in the inoculum, the accumulation of both progeny RNAs was diminished, but near-normal yields of both could be recovered if the inoculum was supplemented with a small, chimeric viral replicon expressing P15, demonstrating that P15 has an effect on viral RNA accumulation. To further analyze the role of P15, transcripts were produced expressing P15 fused to enhanced green fluorescent protein (EGFP). Following inoculation to protoplasts, epifluorescence microscopy revealed that P15 accumulated as spots around the nucleus and in the cytoplasm. Intracellular sites of viral RNA synthesis were visualized by laser scanning confocal microscopy of infected protoplasts labeled with 5-bromouridine 5′-triphosphate (BrUTP). BrUTP labeling also occured in spots distributed within the cytoplasm and around the nucleus. However, the BrUTP-labeled RNA and EGFP/P15 very rarely colocalized, suggesting that P15 does not act primarily at sites of viral replication but intervenes indirectly to control viral accumulation levels.

scholarly journals Novel Antiviral Agent DTriP-22 Targets RNA-Dependent RNA Polymerase of Enterovirus 71

2009 ◽  
Vol 53 (7) ◽  
pp. 2740-2747 ◽  
Author(s):  
Tzu-Chun Chen ◽  
Hwan-You Chang ◽  
Pei-Fen Lin ◽  
Jyh-Haur Chern ◽  
John Tsu-An Hsu ◽  
...  
Keyword(s):  
Potent Inhibitor ◽  
Antiviral Agents ◽  
Enterovirus 71 ◽  
Antiviral Agent ◽  
Viral Rna ◽  
Drug Resistant ◽  
Rna Dependent Rna Polymerase ◽  
Rna Accumulation ◽  
Elongation Activity

ABSTRACT Enterovirus 71 (EV71) has emerged as an important virulent neurotropic enterovirus in young children. DTriP-22 (4{4-[(2-bromo-phenyl)-(3-methyl-thiophen-2-yl)-methyl]-piperazin-1-yl}-1-pheny-1H-pyrazolo[3,4-d]pyrimidine) was found to be a novel and potent inhibitor of EV71. The molecular target of this compound was identified by analyzing DTriP-22-resistant viruses. A substitution of lysine for Arg163 in EV71 3D polymerase rendered the virus drug resistant. DTriP-22 exhibited the ability to inhibit viral replication by reducing viral RNA accumulation. The compound suppressed the accumulated levels of both positive- and negative-stranded viral RNA during virus infection. An in vitro polymerase assay indicated that DTriP-22 inhibited the poly(U) elongation activity, but not the VPg uridylylation activity, of EV71 polymerase. These findings demonstrate that the nonnucleoside analogue DTriP-22 acts as a novel inhibitor of EV71 polymerase. DTriP-22 also exhibited a broad spectrum of antiviral activity against other picornaviruses, which highlights its potential in the development of antiviral agents.

scholarly journals RNA Binding by the Brome Mosaic Virus Capsid Protein and the Regulation of Viral RNA Accumulation

2009 ◽  
Vol 391 (2) ◽  
pp. 314-326 ◽  
Author(s):  
Guanghui Yi ◽  
Robert C. Vaughan ◽  
Ian Yarbrough ◽  
S. Dharmaiah ◽  
C. Cheng Kao
Keyword(s):  
Mosaic Virus ◽  
Capsid Protein ◽  
Rna Binding ◽  
Brome Mosaic Virus ◽  
Viral Rna ◽  
Virus Capsid ◽  
Rna Accumulation ◽  
Virus Capsid Protein

scholarly journals Inhibition of Cellular Autophagy Deranges Dengue Virion Maturation

2012 ◽  
Vol 87 (3) ◽  
pp. 1312-1321 ◽  
Author(s):  
Roberto Mateo ◽  
Claude M. Nagamine ◽  
Jeannie Spagnolo ◽  
Ernesto Méndez ◽  
Michael Rahe ◽  
...  
Keyword(s):  
Dengue Virus ◽  
Virus Production ◽  
Innate Immune ◽  
Viral Rna ◽  
Virus Particles ◽  
Cellular Autophagy ◽  
Autophagy Pathway ◽  
Viral Maturation ◽  
Rna Accumulation ◽  
Selection Of

ABSTRACTAutophagy is an important component of the innate immune response, directly destroying many intracellular pathogens. However, some pathogens, including several RNA viruses, subvert the autophagy pathway, or components of the pathway, to facilitate their replication. In the present study, the effect of inhibiting autophagy on the growth of dengue virus was tested using a novel inhibitor, spautin-1 (specific andpotentautophagyinhibitor 1). Inhibition of autophagy by spautin-1 generated heat-sensitive, noninfectious dengue virus particles, revealing a large effect of components of the autophagy pathway on viral maturation. A smaller effect on viral RNA accumulation was also observed. Conversely, stimulation of autophagy resulted in increased viral titers and pathogenicity in the mouse. We conclude that the presence of functional autophagy components facilitates viral RNA replication and, more importantly, is required for infectious dengue virus production. Pharmacological inhibition of host processes is an attractive antiviral strategy to avoid selection of treatment-resistant variants, and inhibitors of autophagy may prove to be valuable therapeutics against dengue virus infection and pathogenesis.

scholarly journals RNA4-encoded p31 of beet necrotic yellow vein virus is involved in efficient vector transmission, symptom severity and silencing suppression in roots

2007 ◽  
Vol 88 (5) ◽  
pp. 1611-1619 ◽  
Author(s):  
Muhammad Danial Rahim ◽  
Ida Bagus Andika ◽  
Chenggui Han ◽  
Hideki Kondo ◽  
Tetsuo Tamada
Keyword(s):  
Sugar Beet ◽  
Rna Silencing ◽  
Viral Rna ◽  
Yellow Vein ◽  
Symptom Expression ◽  
Suppressor Activity ◽  
Vector Transmission ◽  
Efficient Vector ◽  
Silencing Suppression ◽  
Rna Accumulation

RNA3 and RNA4 of beet necrotic yellow vein virus (BNYVV) are not essential for virus multiplication, but are associated with vector-mediated infection and disease development in sugar beet roots. Here, a unique role for RNA4 in virus transmission, virulence and RNA silencing suppression was demonstrated. Mutagenic analysis revealed that the RNA4-encoded p31 open reading frame (ORF) was involved in efficient vector transmission and slight enhancement of symptom expression in some Beta species. No effects of RNA4 on virus accumulation in infected tissue were observed. Furthermore, the p31 ORF was involved in the induction of severe symptoms by BNYVV in Nicotiana benthamiana plants without affecting viral RNA accumulation. In contrast, RNA3-encoded p25, previously identified as a major contributor to symptom induction in sugar beet, had no such effect on N. benthamiana. In two different silencing suppression assays, neither p31 nor p25 was able to suppress RNA silencing in leaves, but the presence of p31 enhanced a silencing suppressor activity in roots without alteration in viral RNA accumulation. Thus, BNYVV p31 plays a multifunctional role in efficient vector transmission, enhanced symptom expression and root-specific silencing suppression.

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