Complexities of Viral Mutation Rates

Peck, Kayla M.; Lauring, Adam S.

doi:10.1128/jvi.01031-17

Cited by 362 publications

(355 citation statements)

References 47 publications

(80 reference statements)

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“…Essentially, the viral mutation rate and copy number determine the variability within the host and in fine the stock of viral evolution (Duffy et al 2008;Peck and Lauring 2018;Sanjuán and Domingo-Calap 2016). Generally, viral pathogens exist in diverse populations in vivo (McCrone and Lauring 2018).…”

Section: Effects Of the Bottleneck Phenomenonmentioning

confidence: 99%

Virus–Host Coevolution with a Focus on Animal and Human DNA Viruses

et al. 2019

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Viruses have been infecting their host cells since the dawn of life, and this extremely long-term coevolution gave rise to some surprising consequences for the entire tree of life. It is hypothesised that viruses might have contributed to the formation of the first cellular life form, or that even the eukaryotic cell nucleus originates from an infection by a coated virus. The continuous struggle between viruses and their hosts to maintain at least a constant fitness level led to the development of an unceasing arms race, where weapons are often shuttled between the participants. In this literature review we try to give a short insight into some general consequences or traits of virus-host coevolution, and after this we zoom in to the viral clades of adenoviruses, herpesviruses, nucleo-cytoplasmic large DNA viruses, polyomaviruses and, finally, circoviruses.

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Section: Effects Of the Bottleneck Phenomenonmentioning

confidence: 99%

Virus–Host Coevolution with a Focus on Animal and Human DNA Viruses

et al. 2019

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“…Such high mutation rates reflect erroneous genome replication in the absence of any error correction, with only sporadic instances of RNA repair in contrast with what is seen in double-stranded DNA-based organisms (Drake 1993;Drake et al 1998;Bellacosa and Moss 2003). Across RNA viruses as a whole, estimated mutation rates fall within a range of 10 24 -10 26 mutations per site per cell replication (Sanjuán et al 2010;Sanjuán 2012;Peck and Lauring 2018), between different infected cells in the same culture or individual host (Combe et al 2015). Evolutionary rates (that is, the number of fixed substitutions per unit time) range from 10 22 to 10 25 nucleotide substitutions per site per year (Duffy et al 2008;Sanjuán 2012;Holmes et al 2016), and hence are several orders of magnitude greater than those observed in double-stranded DNA organisms (Duffy et al 2008;Sanjuán 2012).…”

Section: An Evolutionary World Shaped By Mutationmentioning

confidence: 99%

“…It is therefore no surprise that RNA viruses comprise the most important class of emerging viruses (Cleaveland et al 2001). More difficult to determine are the selective forces that have shaped the evolution of mutation rates in RNA viruses (Regoes et al 2013;Peck and Lauring 2018). One suggestion is that the genetic diversity produced by frequent mutation is in itself selectively advantageous and may directly contribute to such features as viral pathogenesis (Vignuzzi et al 2006).…”

Section: An Evolutionary World Shaped By Mutationmentioning

confidence: 99%

Evolutionary Virology at 40

Geoghegan

Holmes

2018

Genetics

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RNA viruses are diverse, abundant, and rapidly evolving. Genetic data have been generated from virus populations since the late 1970s and used to understand their evolution, emergence, and spread, culminating in the generation and analysis of many thousands of viral genome sequences. Despite this wealth of data, evolutionary genetics has played a surprisingly small role in our understanding of virus evolution. Instead, studies of RNA virus evolution have been dominated by two very different perspectives, the experimental and the comparative, that have largely been conducted independently and sometimes antagonistically. Here, we review the insights that these two approaches have provided over the last 40 years. We show that experimental approaches using in vitro and in vivo laboratory models are largely focused on short-term intrahost evolutionary mechanisms, and may not always be relevant to natural systems. In contrast, the comparative approach relies on the phylogenetic analysis of natural virus populations, usually considering data collected over multiple cycles of virus-host transmission, but is divorced from the causative evolutionary processes. To truly understand RNA virus evolution it is necessary to meld experimental and comparative approaches within a single evolutionary genetic framework, and to link viral evolution at the intrahost scale with that which occurs over both epidemiological and geological timescales. We suggest that the impetus for this new synthesis may come from methodological advances in next-generation sequencing and metagenomics.

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“…Some of the OPV's strengths (live virus, secondary transmission) are also its biggest weaknesses. Due to their error‐prone RNA‐dependent RNA polymerase, polioviruses (and picornaviruses, in general) evolve extremely rapidly at the nucleotide level, on the order of 1% per year along a chain of transmission . However, approximately 90% of these are synonymous substitutions (i.e., there is no change in the encoded amino acid), so that the same vaccines developed over 60 years ago still provide immunity to the genetically distinct wild viruses that circulate today.…”

mentioning

confidence: 99%

“…Due to their errorprone RNA-dependent RNA polymerase, polioviruses (and picornaviruses, in general) evolve extremely rapidly at the nucleotide level, on the order of 1% per year along a chain of transmission. 11 However, approximately 90% of these are synonymous substitutions (i.e., there is no change in the encoded amino acid), so that the same vaccines developed over 60 years ago still provide immunity to the genetically distinct wild viruses that circulate today. OPV strains were derived by serial passage of WPVs in cell culture and/or nonhuman primates, resulting in attenuation of replication efficiency as well as neurovirulence.…”

mentioning

confidence: 99%

Progress of polio eradication and containment requirements after eradication

Oberste

2018

Transfusion

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Wild poliovirus (WPV) is nearing eradication, and only three countries have never interrupted WPV transmission (Pakistan, Afghanistan, and Nigeria). WPV2 was last detected in 1999, and it was declared eradicated in 2015. WPV3 has not been detected since 2012. Since 2016, WPV1 has been detected in only two countries (Afghanistan and Pakistan), with only 22 cases reported in 2017 and 12 cases reported in 2018 (as of July 10). Because of WPV2 eradication and the risk of emergence of type 2 vaccine–derived polioviruses from continued use of trivalent oral polio vaccine (OPV), trivalent OPV was replaced by bivalent OPV (types 1 and 3) in a globally coordinated effort in 2016. WPV2 eradication and trivalent OPV cessation also mean that breach of containment in a facility working with type 2 poliovirus is now a major risk to reseed type 2 circulation in the community. As a result, the World Health Organization has developed a “Global Action Plan to minimize poliovirus facility‐associated risk after type‐specific eradication of wild polioviruses and sequential cessation of oral polio vaccine use.” Because poliovirus has long been used as a standard for qualification of intravenous immunoglobulin, disinfectant products, and sanitation methods, poliovirus containment has implications far beyond poliovirus laboratories.

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Complexities of Viral Mutation Rates

Cited by 362 publications

References 47 publications

Virus–Host Coevolution with a Focus on Animal and Human DNA Viruses

Virus–Host Coevolution with a Focus on Animal and Human DNA Viruses

Evolutionary Virology at 40

Progress of polio eradication and containment requirements after eradication

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