Animal and human RNA viruses: genetic variability and ability to overcome vaccines
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MINI-REVIEW
Animal and human RNA viruses: genetic variability and ability to overcome vaccines T. G. Villa1 · Ana G. Abril1 · S. Sánchez1 · T. de Miguel1 · A. Sánchez‑Pérez2 Received: 18 April 2020 / Revised: 29 June 2020 / Accepted: 12 September 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract RNA viruses, in general, exhibit high mutation rates; this is mainly due to the low fidelity displayed by the RNA-dependent polymerases required for their replication that lack the proofreading machinery to correct misincorporated nucleotides and produce high mutation rates. This lack of replication fidelity, together with the fact that RNA viruses can undergo spontaneous mutations, results in genetic variants displaying different viral morphogenesis, as well as variation on their surface glycoproteins that affect viral antigenicity. This diverse viral population, routinely containing a variety of mutants, is known as a viral ‘quasispecies’. The mutability of their virions allows for fast evolution of RNA viruses that develop antiviral resistance and overcome vaccines much more rapidly than DNA viruses. This also translates into the fact that pathogenic RNA viruses, that cause many diseases and deaths in humans, represent the major viral group involved in zoonotic disease transmission, and are responsible for worldwide pandemics. Keywords RNA viruses · Viral RNA polymerases · Viral genetic variability · Viral vaccines
Introduction Animal RNA viruses, in general, exhibit high mutation rates; according to Combe and Sanjuán (2014), the frequency of new mutations in these virions ranges from 10–4 to 10–6 substitutions per nucleotide per round of copying, with transitions more common than transversions. In addition, the mutation process is also affected by the host cells, with VSV mutating at a significantly higher rate in mammalian cells than in insect cells. Other factors affecting the frequency of mutation are the viral family, the polarity of the RNA (+ or positive-sense, 5′-to-3′;—or negative-sense, 3′-to-5′), and whether the genome is single-stranded (ssRNA) or doublestranded (dsRNA). The RNA-dependent RNA polymerases in these viruses lack the proofreading machinery to correct Communicated by Erko stackebrandt. * T. G. Villa [email protected] 1
Department of Microbiology, Faculty of Pharmacy, University of Santiago de Compostela, 5706 Santiago de Compostela, Spain
Sydney School of Veterinary Science, Faculty of Science, University of Sydney, Sydney, NSW 2006, Australia
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misincorporated nucleotides, which often results in a high generation of mutated phenotypes. This means that RNA viruses exhibit good abilities to overcome the pressure of either vaccines or antiviral drugs; these viruses have an advantage over DNA viruses in this regard, as the latter contain proofreading mechanisms. Even if infection is initiated by a single pathogenic RNA-containing unit, after a few rounds of replication, the viral population routinely contains a variety of mutants (known as “the mutant sw
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