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. 2014 Nov 12;9(11):e112129.
doi: 10.1371/journal.pone.0112129. eCollection 2014.

Molecular epidemiology of seal parvovirus, 1988-2014

Affiliations

Molecular epidemiology of seal parvovirus, 1988-2014

Rogier Bodewes et al. PLoS One. .

Abstract

A novel parvovirus was discovered recently in the brain of a harbor seal (Phoca vitulina) with chronic meningo-encephalitis. Phylogenetic analysis of this virus indicated that it belongs to the genus Erythroparvovirus, to which also human parvovirus B19 belongs. In the present study, the prevalence, genetic diversity and clinical relevance of seal parvovirus (SePV) infections was evaluated in both harbor and grey seals (Halichoerus grypus) that lived in Northwestern European coastal waters from 1988 to 2014. To this end, serum and tissue samples collected from seals were tested for the presence of seal parvovirus DNA by real-time PCR and the sequences of the partial NS gene and the complete VP2 gene of positive samples were determined. Seal parvovirus DNA was detected in nine (8%) of the spleen tissues tested and in one (0.5%) of the serum samples tested, including samples collected from seals that died in 1988. Sequence analysis of the partial NS and complete VP2 genes of nine SePV revealed multiple sites with nucleotide substitutions but only one amino acid change in the VP2 gene. Estimated nucleotide substitution rates per year were 2.00 × 10(-4) for the partial NS gene and 1.15 × 10(-4) for the complete VP2 gene. Most samples containing SePV DNA were co-infected with phocine herpesvirus 1 or PDV, so no conclusions could be drawn about the clinical impact of SePV infection alone. The present study is one of the few in which the mutation rates of parvoviruses were evaluated over a period of more than 20 years, especially in a wildlife population, providing additional insights into the genetic diversity of parvoviruses.

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Conflict of interest statement

Competing Interests: One author of the manuscript has interests to declare: Prof. Dr. ADME Osterhaus is part time chief scientific officer of Viroclinics Biosciences B.V. There are no patents, products in development or marketed products to declare. This does not alter the authors' adherence to PLOS ONE policies on sharing data and materials. The other authors have no competing interests to declare.

Figures

Figure 1
Figure 1. Variation in SePV sequences.
Schematic overview of the partial NS gene and the complete VP2 gene that was amplified of 9 SePV variants. The consensus sequence of each virus was compared to the oldest sample available (HSePV-PV880823.6). Locations with nucleotide mutations are indicated in grey. Only in sample HSePV-121216.01, a nucleotide mutation resulted in an amino acid substitution (S540T).
Figure 2
Figure 2. Maximum likelihood tree of the VP2 gene and partial NS1 gene of SePV.
Phylogenetic maximum-likelihood tree with 500 bootstrap replicates of the nucleotide sequence of the VP2 genes (A) and partial NS genes (B) of SePV variants and various viruses of the genus Erythroparvovirus. Only bootstrap values >70 are indicated. Genbank accession numbers: SePV-HG06130: KM252691, SePV-HG020628.02: KM252694, SePV-PV121216.01: KM252698, SePV-PV880823.6: KM252692, SePV-PV880927.20: KM252693, SePV12410: KF373759, SePV-PV020628.13: KM252695, SePV-PV020718.12: KM252696, SePV-PV020719.08: KM252697, bovine parvovirus 3: AF406967, chipmunk parvovirus: GQ200736, rhesus macaque parvovirus: AF221122, simian parvovirus: U26342, pig-tailed macaque parvovirus: AF221123, human parvovirus B19-Au: M13178, human parvovirus B19-LaLi: AY044266, human parvovirus B19-V9: AJ249437.

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