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.

Canine parvovirus (CPV) is an emerging DNA virus that was first observed to cause disease in canines in 1978 and has since become a ubiquitous pathogen worldwide. CPV emerged from feline panleukopenia parvovirus (FPLV) or a closely related virus, differing at several key amino acid residues. Here we characterize the evolutionary processes underlying the emergence of CPV. Although FPLV has remained an endemic infection in its host populations, we show that, since the 1970s, the newly emerged CPV has undergone an epidemic-like pattern of logistic͞exponential growth, effectively doubling its population size every few years. This rapid population growth was associated with a lineage of CPV that acquired a broader host range and greater infectivity. Recombination played no role in the emergence of CPV. Rather, any preexisting variation in the donor species and the subsequent rapid adaptation of the virus to canines were likely dependent on a high rate of mutation and the positive selection of mutations in the major capsid gene. Strikingly, although these single-stranded viruses have a DNA genome and use cellular replication machinery, their rate of nucleotide substitution is closer to that of RNA viruses than to that of double-stranded DNA viruses.adaptation ͉ emergence ͉ mutation rate ͉ phylogeny ͉ natural selection P arvoviruses (family Parvoviridae) are small eukaryotic DNA viruses that infect a variety of animal species, including humans. Canine parvovirus (CPV), feline panleukopenia virus (FPLV), and a number of viruses similar to FPLV, such as blue fox parvovirus, the raccoon parvoviruses, and mink enteritis virus (MEV), are all host-range variants of the carnivore parvovirus subgroup (1, 2). Both disease and pathology differ depending on the age of the infected animal, because the viruses replicate only in cells in the S phase of the cell cycle. In neonatal animals, the virus replicates in a large number of tissues, and FPLV often causes cerebellar hypoplasia, whereas CPV causes myocarditis. In older animals, viral replication is limited to lymphoid and small intestinal cells, causing temporary panleukopenia or lymphopenia (3). FPLV is thought to have been endemic in felines since before the beginning of the 20th century (4). In contrast, it was not until 1978 that CPV (the first known strain was designated CPV2) was observed in canines, having emerged from FPLV or one of the closely related carnivore parvoviruses. Although CPV2 infected feline cells in culture, it did not infect cats. CPV2 was later replaced by a new lineage, designated CPV2a, which, along with its variants, can infect both dogs and cats (5, 6). There is also evidence that CPV2a is more effective at infecting canine cells than is CPV2 (7).Although epidemiological studies of emerging viruses are commonplace, the evolutionary processes associated with crossspecies virus transfer are poorly understood. Under some models, adaptation to the new host species is of fundamental importance, elevating the reproductive rate of the virus (R 0 ) above the...