Parvovirus host range, cell tropism and evolution

Hueffer, Karsten; Parrish, Colin R.

doi:10.1016/s1369-5274(03)00083-3

Cited by 172 publications

(147 citation statements)

References 48 publications

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“…There is also concern that the newer antigenic variants may cause a more severe disease than the original CPV-2 (Carmichael, 2005). These changes in the biological behaviour may be associated with the improved ability of CPV-2a and CPV-2b to bind to the transferrin receptor in comparison with the original type 2 (Hueffer & Parrish, 2003). In contrast, FPLV since its first identification in 1920 has not undergone significant changes in antigenic and biological properties.…”

Section: Discussionmentioning

confidence: 99%

Genetic analysis of feline panleukopenia viruses from cats with gastroenteritis

Decaro¹,

Desario²,

Miccolupo

et al. 2008

Journal of General Virology

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Thirty-nine parvovirus strains contained in faecal samples collected in Italy (n534) and UK (n55) from cats with feline panleukopenia were characterized at the molecular level. All viruses were proven to be true feline panleukopenia virus (FPLV) strains by a minor groove binder probe assay, which is able to discriminate between FPLV and the closely related canine parvovirus type 2. By using sequence analysis of the VP2 gene, it was found that the FPLV strains detected in Italy and UK were highly related to each other, with a nucleotide identity of 99.1-100 and 99.4-99.8 % among Italian and British strains, respectively, whereas the similarities between all the sequences analysed were 98.6-100 %. Eighty-eight variable positions were detected in the VP2 gene of the field and reference FPLV strains, most of which were singletons. Synonymous substitutions (n557) predominated over non-synonymous substitutions (n531), and the ratio between synonymous and non-synonymous substitutions (dN/dS) was 0.10, thus confirming that evolution of FPLV is driven by random genetic drift rather than by positive selection pressure. Some amino acid mutations in the VP2 protein affected sites that are thought to be responsible for antigenic and biological properties of the virus, but no clear patterns of segregation and genetic markers, were identified, confirming that FPLV is in evolutionary stasis.

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Section: Discussionmentioning

confidence: 99%

Genetic analysis of feline panleukopenia viruses from cats with gastroenteritis

Decaro¹,

Desario²,

Miccolupo

et al. 2008

Journal of General Virology

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“…The emergent canine parvoviruses are characterized by specific amino acid changes in and around a raised region of the capsid termed the threefold spike. Structural and mutational studies suggest that this region binds the cellular transferrin receptor and controls host range (7,12). This capsid region is also highly antigenic, serving as the target of many neutralizing antibodies.…”

mentioning

confidence: 99%

High rate of viral evolution associated with the emergence of carnivore parvovirus

Shackelton

Parrish

Truyen

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

486

387

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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...

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“…Understanding host range evolution in E150 The American Naturalist phages also has implications for eukaryotic viruses. Host shifts in mammalian viruses have caused devastating epidemics (Sharp et al 2001;Truyen 2006), and the evolution of new tissue tropisms within a host (which can be considered a form of host range evolution) is important in some diseases (Hueffer and Parrish 2003). Understanding viral evolution to avoid/infect certain tissues is thus important to understanding the nature of within-host viral adaptation and the balance between adaptation for maximum transmission and adaptation within the host (Zhang et al 1993).…”

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confidence: 99%