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1 Enterovirus Laboratory, Department of Microbiology, National Public Health Institute (KTL), Mannerheimintie 166, 00300 Helsinki, Finland
2 Centers for Disease Control and Prevention (CDC), Atlanta, Georgia, USA
Correspondence
Tapani Hovi
tapani.hovi{at}ktl.fi
Wild-type 1 poliovirus (wtPV1) strains were isolated from two young healthy brothers shortly after arrival in Finland from Somalia in 1993. Twelve (sibling A) and 18 (sibling B) specimens collected over a period of more than 6 months yielded wtPV1. Partial sequences obtained from the one and two earliest isolates from sibling A and B, respectively, were nearly identical, differing from each other by only one or two nucleotides. Subsequently, the virus evolved separately in both siblings so that maximal differences between strains derived from a given subject peaked at 2·2 % for sibling A, at 1·5 % for sibling B and at 2·5 % between the two siblings in the VP1-coding part of the genome. All substitutions in the 150 nt VP1–2A junction region were synonymous, whereas as many as eight of the 31 variable positions in the remaining VP1-coding region encoded amino acid replacements in at least one strain. Probable structural locations of the variable amino acid positions were mapped to the published PV1/Mahoney structural model. Most of the substitutions occurred around the fivefold axis in motifs that are known to be or suspected to be targets of neutralizing antibodies. We suggest that the striking genetic divergence observed between the strains was based on a combination of bottleneck transmission events and antigenic drift during the prolonged period of poliovirus replication.
The sequences obtained in this study have been assigned GenBank accession nos AY323842–AY323852.
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