RNA Viruses and RNAi: Quasispecies Implications for Viral Escape

Presloid, John B.; Novella, Isabel S.

doi:10.3390/v7062768

Cited by 29 publications

(30 citation statements)

References 97 publications

(98 reference statements)

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“…This mutation, close to the 5′ end of amiR‐TSWV, may affect target slicing, whereas the second most frequent mutation, C4068A, inducing a central mismatch may trigger translation repression of TSWV‐L RNA. In any case, RNAi viral escapees with altered TS sequences have also been observed in human viruses such as polio virus , Hepatitis C virus , HIV and Japanese encephalitis virus (JEV), and also in animal viruses such as the model morbillivirus Peste des petits ruminants virus (PPRV) (Presloid and Novella, ). Still, resistance mutations may not always be located in TSs, suggesting that different mechanisms can be used to escape RNAi (Berkhout and Das, ; Shah et al ., ).…”

Section: Discussionmentioning

confidence: 99%

“…Here, the most frequent mutation in TSs from the region 4058-4078 of TSWV segment L is U4074C, which was observed in 10 of the 12 independent progenies. This mutation, close to the 5 0 end of amiR-TSWV, may affect in animal viruses such as the model morbillivirus Peste des petits ruminants virus (PPRV) (Presloid and Novella, 2015). Still, resistance mutations may not always be located in TSs, suggesting that different mechanisms can be used to escape RNAi (Berkhout and Das, 2012;Shah et al, 2012).…”

Section: Subinhibitory Accumulation Of Amir-tswv Allows Virus Evasionmentioning

confidence: 99%

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Multi‐targeting of viral RNAs with synthetic trans‐acting small interfering RNAs enhances plant antiviral resistance

2019

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Summary RNA interference (RNAi)‐based tools are used in multiple organisms to induce antiviral resistance through the sequence‐specific degradation of target RNAs by complementary small RNAs. In plants, highly specific antiviral RNAi‐based tools include artificial microRNAs (amiRNAs) and synthetic trans‐acting small interfering RNAs (syn‐tasiRNAs). syn‐tasiRNAs have emerged as a promising antiviral tool allowing for the multi‐targeting of viral RNAs through the simultaneous expression of several syn‐tasiRNAs from a single precursor. Here, we compared in tomato plants the effects of an amiRNA construct expressing a single amiRNA and a syn‐tasiRNA construct expressing four different syn‐tasiRNAs against Tomato spotted wilt virus (TSWV), an economically important pathogen affecting tomato crops worldwide. Most of the syn‐tasiRNA lines were resistant to TSWV, whereas the majority of the amiRNA lines were susceptible and accumulated viral progenies with mutations in the amiRNA target site. Only the two amiRNA lines with higher amiRNA accumulation were resistant, whereas resistance in syn‐tasiRNA lines was not exclusive of lines with high syn‐tasiRNA accumulation. Collectively, these results suggest that syn‐tasiRNAs induce enhanced antiviral resistance because of the combined silencing effect of each individual syn‐tasiRNA, which minimizes the possibility that the virus simultaneously mutates all different target sites to fully escape each syn‐tasiRNA.

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Section: Discussionmentioning

confidence: 99%

Section: Subinhibitory Accumulation Of Amir-tswv Allows Virus Evasionmentioning

confidence: 99%

Multi‐targeting of viral RNAs with synthetic trans‐acting small interfering RNAs enhances plant antiviral resistance

2019

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“…Obviously, the regularities discussed in this review are important not only for a deeper understanding of certain fundamental aspects of the lifestyle of RNA viruses but also for numerous applied problems, such as the efficiency of antiviral tools and the development of drug resistance (533)(534)(535)(536)(537). For the first several years of his career, he participated in studies of various aspects of the cap-independent translation of picornavirus RNAs.…”

Section: Robustness Resilience and Evolvability Of Viral Rna Genomesmentioning

confidence: 99%

Emergency Services of Viral RNAs: Repair and Remodeling

Agol

Gmyl

2018

Microbiol Mol Biol Rev

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Reproduction of RNA viruses is typically error-prone due to the infidelity of their replicative machinery and the usual lack of proofreading mechanisms. The error rates may be close to those that kill the virus. Consequently, populations of RNA viruses are represented by heterogeneous sets of genomes with various levels of fitness. This is especially consequential when viruses encounter various bottlenecks and new infections are initiated by a single or few deviating genomes. Nevertheless, RNA viruses are able to maintain their identity by conservation of major functional elements. This conservatism stems from genetic robustness or mutational tolerance, which is largely due to the functional degeneracy of many protein and RNA elements as well as to negative selection. Another relevant mechanism is the capacity to restore fitness after genetic damages, also based on replicative infidelity. Conversely, error-prone replication is a major tool that ensures viral evolvability. The potential for changes in debilitated genomes is much higher in small populations, because in the absence of stronger competitors low-fit genomes have a choice of various trajectories to wander along fitness landscapes. Thus, low-fit populations are inherently unstable, and it may be said that to run ahead it is useful to stumble. In this report, focusing on picornaviruses and also considering data from other RNA viruses, we review the biological relevance and mechanisms of various alterations of viral RNA genomes as well as pathways and mechanisms of rehabilitation after loss of fitness. The relationships among mutational robustness, resilience, and evolvability of viral RNA genomes are discussed.

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“…The indirect impact of virus over cells morphology (CPE and IFA) virus titer, virus copy number in si5U and si3D pol transfected cells shown their full resistance for propagation of CA24.All experiments were performed in 3 biological and 3 technical replicates for consistency of obtained data (p<0.05). The error-prone replication mechanism and high mutation rate of RNA viruses allows them to readily escape from RNAi and emergence of [27]. In case of escape mutants, targeting several regions of virus at a time in the form of combination therapy of siRNA cocktail may provide better protection from virus effect.…”

Section: Discussionmentioning

confidence: 99%