Abstract
During the past decade the role of genetic variation during RNA virus replication has gained increased attention as a strategy for viral persistence. Through mechanisms such as genomic point mutations, recombination, and reassortment of multipartite genomes, RNA viruses are capable of modifying their genetic constitution, often resulting in altered biologic (host cell specificity, pathogenicity) or immunologic properties (Holland et al., 1982). The propensity for variation among animal RNA viruses by mutation is usually attributed to the relatively high infidelity of virus-encoded RNA polymerases that replicate the viral genome. Compared to DNA polymerases that display error rates of 10-8 to 10-11 nucleotide substitutions per site per year, viral RNA polymerases reveal mutation rates of about 10-4 to 10-5. Moreover, the genetic variations introduced during viral RNA replication in the cell cytoplasm tend to accumulate, as RNA polymerases lack the editing and repair functions typically associated with nuclear DNA polymerases. Thus, RNA viruses appear to constitute a highly variable system of genetic information in which nature is constantly experimenting with novel genetic constitutions.
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Montelaro, R., Ball, J., Rwambo, P., Issel, C. (1989). Antigenic Variation during Persistent Lentivirus Infections and Its Simplications for Vaccine Development. In: Atassi, M.Z. (eds) Immunobiology of Proteins and Peptides V. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-2046-4_24
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