Residues in the Apical Domain of the Feline and Canine Transferrin Receptors Control Host-Specific Binding and Cell Infection of Canine and Feline Parvoviruses

Palermo, Laura M.; Hueffer, Karsten; Parrish, Colin R.

doi:10.1128/jvi.77.16.8915-8923.2003

Cited by 69 publications

(114 citation statements)

References 43 publications

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“…*Nd N͞SdS ϭ total nonsynonymous changes͞total synonymous changes. region of contact with the transferrin receptor (12,38,40). Furthermore, both residue 93 and the 300 region are within binding sites for many neutralizing antibodies (41).…”

Section: Discussionmentioning

confidence: 99%

“…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.…”

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confidence: 99%

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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.

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485

384

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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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Section: Discussionmentioning

confidence: 99%

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.

Self Cite

485

384

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“…Whereas both viruses can use feline TfR to enter cells, CPV has gained the ability to bind canine TfR, albeit at a lower affinity (13). Residues that are involved in host-range control and specific recognition of TfR are on the viral surface in the vicinity of the spikes (6,14).…”

mentioning

confidence: 99%

“…Each monomer has a carboxypeptidase-like domain, an apical domain, and a helical domain. Mutagenesis of feline and canine TfR indicates that CPV and feline panleukopenia virus bind to the apical domain of the receptor, distal from the membrane-binding region (14).…”

mentioning

confidence: 99%

Asymmetric binding of transferrin receptor to parvovirus capsids

Hafenstein

Palermo

Kostyuchenko

et al. 2007

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

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Although many viruses are icosahedral when they initially bind to one or more receptor molecules on the cell surface, such an interaction is asymmetric, probably causing a breakdown in the symmetry and conformation of the original infecting virion in preparation for membrane penetration and release of the viral genome. Cryoelectron microscopy and biochemical analyses show that transferrin receptor, the cellular receptor for canine parvovirus, can bind to only one or a few of the 60 icosahedrally equivalent sites on the virion, indicating that either canine parvovirus has inherent asymmetry or binding of receptor induces asymmetry. The asymmetry of receptor binding to canine parvovirus is reminiscent of the special portal in tailed bacteriophages and some large, icosahedral viruses. Asymmetric interactions of icosahedral viruses with their hosts might be a more common phenomenon than previously thought and may have been obscured by averaging in previous crystallographic and electron microscopic structure determinations.asymmetric reconstruction ͉ canine parvovirus ͉ receptor-virus interaction ͉ unique binding

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“…Canine parvovirus (CPV) and feline panleukopenia virus (FPV) capsids bind to the transferrin receptors (TfRs) of their hosts and use these receptors to infect cells. The binding is partially host specific, as FPV binds only to the feline TfR, while CPV binds to both the canine and feline TfRs [5]. difference between CPV types 2a and 2b is the presence of two single nucleotide polymorphisms (SNPs) in the capsid protein gene sequence, which determines amino acid changes in the major antigenic sites of the viral capsid [11].…”

Section: Molecular Characteristic Of Canine Parvovirus Typementioning

confidence: 99%

Isolation and Molecular Characterization of Canine and Feline Parvovirus Strains - An Updated Review

Brindhalakshmi¹

2016

JDVAR

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Residues in the Apical Domain of the Feline and Canine Transferrin Receptors Control Host-Specific Binding and Cell Infection of Canine and Feline Parvoviruses

Cited by 69 publications

References 43 publications

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

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

Asymmetric binding of transferrin receptor to parvovirus capsids

Isolation and Molecular Characterization of Canine and Feline Parvovirus Strains - An Updated Review

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