Mechanisms of viral mutation

Sanjuán, Rafael; Domingo‐Calap, Pilar

doi:10.1007/s00018-016-2299-6

Cited by 732 publications

(673 citation statements)

References 171 publications

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“…See text for DNA virus mutation rate references. Details on mutation rate data can be found in a recent review [26]. Bacterial and viroid mutation rates were taken from a previous review [7].…”

Section: Discussionmentioning

confidence: 99%

Genome-Wide Estimation of the Spontaneous Mutation Rate of Human Adenovirus 5 by High-Fidelity Deep Sequencing

2016

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Rates of spontaneous mutation determine the ability of viruses to evolve, infect new hosts, evade immunity and undergo drug resistance. Contrarily to RNA viruses, few mutation rate estimates have been obtained for DNA viruses, because their high replication fidelity implies that new mutations typically fall below the detection limits of Sanger and standard next-generation sequencing. Here, we have used a recently developed high-fidelity deep sequencing technique (Duplex Sequencing) to score spontaneous mutations in human adenovirus 5 under conditions of minimal selection. Based on >200 single-base spontaneous mutations detected throughout the entire viral genome, we infer an average mutation rate of 1.3 × 10−7 per base per cell infection cycle. This value is similar to those of other, large double-stranded DNA viruses, but an order of magnitude lower than those of single-stranded DNA viruses, consistent with the possible action of post-replicative repair. Although the mutation rate did not vary strongly along the adenovirus genome, we found several sources of mutation rate heterogeneity. First, two regions mapping to transcription units L3 and E1B-IVa2 were significantly depleted for mutations. Second, several point insertions/deletions located within low-complexity sequence contexts appeared recurrently, suggesting mutational hotspots. Third, mutation probability increased at GpC dinucleotides. Our findings suggest that host factors may influence the distribution of spontaneous mutations in human adenoviruses and potentially other nuclear DNA viruses.

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Section: Discussionmentioning

confidence: 99%

Genome-Wide Estimation of the Spontaneous Mutation Rate of Human Adenovirus 5 by High-Fidelity Deep Sequencing

2016

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“…These include the complex structures of respiratory viruses, the variety of viral surface proteins essential for infection, the different pathways important for infection and the fact that viruses mutate frequently that may result in treatment difficulty [6]. It could be beneficial to design treatments to act topically on the surface of the oropharynx as most cold viruses are present on the throat's outer lining during infection [7].…”

Section: Introductionmentioning

confidence: 99%

A medical device forming a protective barrier that deactivates four major common cold viruses

Stefansson¹,

Guðmundsdóttir²,

Clarsund³

2017

Virol Res Rev

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The medical device ColdZyme is a mouth spray that forms a barrier in the throat against common cold viruses. The barrier solution of the device is composed of glycerol and Atlantic cod trypsin. The aim of this study was to evaluate the virus deactivating ability of ColdZyme against four major common cold viruses. A virucidal efficacy suspension test was conducted using ColdZyme against each of the challenge viruses in suspension. ColdZyme deactivated rhinovirus type 1A by 91.7% (1.08 log 10 ), rhinovirus type 42 by 92.8% (1.14 log 10 ), human influenza A virus H3N2 by 96.9% (1.51 log 10 ), respiratory syncytial virus (RSV) by 99.9% (2.94 log 10 ) and adenovirus type 2 by 64.5% (0.45 log 10 ). Based on the results, ColdZyme showed an effective broad-spectrum impact against common cold viruses. Thus, ColdZyme might represent a device with clinical benefits in prevention and treatment of respiratory viral infections by deactivating viruses within the respiratory tract.

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“…These target EUs displayed a diverse range of sequence similarity (13.5%‐100% HHpred probability) and structure similarity (23.5‐89.4 LGA_S) to known folds. Examples of H‐group assignments with low sequence scores include domains from virus or phage that are known for fast evolution, such as the pectin lyase‐like single‐stranded, right‐handed beta‐helix domain in T0953s2‐D2, the phage tail protein‐like domain in T1021s3‐D1 and T1021s3‐D2, the Phi ETA orf 56‐like protein C‐terminal domain in T0989‐D2, and others, the Phage tail fiber protein trimerization domain in T0953s1, or the RNA bacteriophage capsid protein in T0998. Similarly, fast evolving domains, like RelE‐like toxin domains (T0957s1‐D1, T0968s1, and T0980s1) or colicin D nuclease domain (T0986s1) are involved in bacterial resistance or toxicity.…”

Section: Resultsmentioning

confidence: 99%

CASP13 target classification into tertiary structure prediction categories

et al. 2019

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Protein target structures for the Critical Assessment of Structure Prediction round 13 (CASP13) were split into evaluation units (EUs) based on their structural domains, the domain organization of available templates, and the performance of servers on whole targets compared to split target domains. Eighty targets were split into 112 EUs. The EUs were classified into categories suitable for assessment of high accuracy modeling (or template‐based modeling [TBM]) and topology (or free modeling [FM]) based on target difficulty. Assignment into assessment categories considered the following criteria: (a) the evolutionary relationship of target domains to existing fold space as defined by the Evolutionary Classification of Protein Domains (ECOD) database; (b) the clustering of target domains using eight objective sequence, structure, and performance measures; and (c) the placement of target domains in a scatter plot of target difficulty against server performance used in the previous CASP. Generally, target domains with good server predictions had close template homologs and were classified as TBM. Alternately, targets with poor server predictions represent a mixture of fast evolving homologs, structure analogs, and new folds, and were classified as FM or FM/TBM overlap.

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Mechanisms of viral mutation

Cited by 732 publications

References 171 publications

Genome-Wide Estimation of the Spontaneous Mutation Rate of Human Adenovirus 5 by High-Fidelity Deep Sequencing

Genome-Wide Estimation of the Spontaneous Mutation Rate of Human Adenovirus 5 by High-Fidelity Deep Sequencing

A medical device forming a protective barrier that deactivates four major common cold viruses

CASP13 target classification into tertiary structure prediction categories

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