Differential recognition of the ORF2 region in a complete genome sequence of porcine circovirus type 2 (PCV2) isolated from boar bone marrow in Korea

Porcine circovirus type 2 (PCV2) is the causative agent of post-weaning multisystemic wasting syndrome (PMWS) in swine. Here, a phylogenetic tree was constructed using PCV2 nucleotide sequences derived from the bone marrow of Korean boar and previously reported PCV2 sequences isolated from various c...

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Veröffentlicht in:Gene 2015-09, Vol.569 (2), p.308-312
Hauptverfasser: Kweon, Chang-Hee, Nguyen, Lien Thi Kim, Yoo, Mi-Sun, Kang, Seung-Won
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Sprache:eng
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Zusammenfassung:Porcine circovirus type 2 (PCV2) is the causative agent of post-weaning multisystemic wasting syndrome (PMWS) in swine. Here, a phylogenetic tree was constructed using PCV2 nucleotide sequences derived from the bone marrow of Korean boar and previously reported PCV2 sequences isolated from various countries. PCV2 from Korean boar bone marrow (KC188796) was classified into the group containing PCV2a-Canada and other PCV2 strain from Korea. While the ORF1 region of the PCV2 genome was highly conserved, ORF2 (the capsid protein coding region) was relatively variable. The nucleotide sequences for bone marrow-derived PCV2 were 93.4–99.0% homologous to the other reference sequences. The deduced amino acid sequences for the ORF1 and ORF2 coding regions were 97.4–99.3% and 84.5–97.4% homologous with the other reference strains, respectively, indicating that KC188796 did not differ markedly from the other PCV2 strains. Phylogenetic analysis demonstrated that bone marrow-derived PCV2 was highly similar to PCV2a from Canada and may be related to persistent PCV2 infections in swine. The pig with post-weaning multisystemic wasting syndrome (PMWS). [Display omitted] •The phylogenetic characterization of bone marrow-derived PCV2•The comparative investigation with available genetic resources through the world•The molecular mechanism with reference to persistent infection of PCV2 in swine
ISSN:0378-1119
1879-0038
DOI:10.1016/j.gene.2015.04.055