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dc.contributor.authorVilla, T. G.en_AU
dc.contributor.authorAbril, Ana G.en_AU
dc.contributor.authorSánchez, S.en_AU
dc.contributor.authorde Miguel, T.en_AU
dc.contributor.authorSánchez-Pérez, A.en_AU
dc.date.accessioned2020-10-15
dc.date.available2020-10-15
dc.date.issued2020en_AU
dc.identifier.urihttps://hdl.handle.net/2123/23590
dc.description.abstractRNA 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.en_AU
dc.language.isoenen_AU
dc.subjectCOVID-19en_AU
dc.subjectCoronavirusen_AU
dc.titleAnimal and human RNA viruses: genetic variability and ability to overcome vaccinesen_AU
dc.typeArticleen_AU
dc.identifier.doi10.1007/s00203-020-02040-5


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