Rates of evolutionary change in viruses: patterns and determinants

Abstract

Understanding the factors that determine the rate at which genomes generate and fix mutations provides important insights into key evolutionary mechanisms. We review our current knowledge of the rates of mutation and substitution, as well as their determinants, in RNA viruses, DNA viruses and retroviruses. We show that the high rate of nucleotide substitution in RNA viruses is matched by some DNA viruses, suggesting that evolutionary rates in viruses are explained by diverse aspects of viral biology, such as genomic architecture and replication speed, and not simply by polymerase fidelity.

Increased substitution rate in H5N1 avian influenza viruses during mass vaccination of poultry

“…This is also consistent with previous reports that many amino acid substitutions in the HA1 subunit of H5N1 HPAI viruses occurred at antigenic sites [3,25,40]. In addition, it has also been found by others that the substitution rate of viruses may be elevated by selection of immune escape [41,42]. As mass vaccination programs should lose efficacy with the emergence of vaccine-resistant strains, caution must be taken when adopting mass vaccination as a long-term strategy to control HPAI.…”

Cooperation between different RNA virus genomes produces a new phenotype

“…A n RNA virus population generally evolves rapidly under selection pressure, because of the high error rate of viral RNA polymerase [1][2][3][4][5] . This feature of RNA viruses is thought to have an important role in viral pathogenesis and survival under selection pressure, exemplified in the evolution of the human immunodeficiency virus and the hepatitis C virus 3,[5][6][7] .…”

Human APOBEC3G-Mediated Editing Can Promote HIV-1 Sequence Diversification and Accelerate Adaptation to Selective Pressure

“…HIV-1 is constantly exposed to sequence changes because of a combination of rapid rates of viral replication, poor fidelity of the virus replicating enzymes (reverse transcriptase [RT] and RNA polymerase II), and recombination during simultaneous infection with multiple virus strains (5,6,17,19,21). In addition, mutation of HIV-1 by human APOBEC3G (A3G), a naturally expressed host nucleic acid-editing enzyme that deaminates deoxycytidine to deoxyuridine in the (mostly) minus strand of newly synthesized HIV-1 DNA, may further contribute to viral sequence change (1,2,9,10,15,16,31).…”