Hovi Tapani, Lindholm Noora, Savolainen Carita, Stenvik Mirja, Burns Cara
Enterovirus Laboratory, Department of Microbiology, National Public Health Institute (KTL), Mannerheimintie 166, 00300 Helsinki, Finland.
Centers for Disease Control and Prevention (CDC), Atlanta, Georgia, USA.
J Gen Virol. 2004 Feb;85(Pt 2):369-377. doi: 10.1099/vir.0.19518-0.
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.
1993年，野生型1型脊髓灰质炎病毒（wtPV1）毒株从两名刚从索马里抵达芬兰的健康年幼兄弟身上分离出来。在6个多月的时间里收集的12份（兄弟A）和18份（兄弟B）样本中检测出wtPV1。分别从兄弟A和B最早的一份和两份分离株中获得的部分序列几乎相同，彼此之间仅相差一两个核苷酸。随后，病毒在两兄弟体内分别进化，使得来自同一受试者的毒株之间的最大差异在兄弟A中达到2.2%，在兄弟B中达到1.5%，在基因组VP1编码部分两兄弟的毒株之间达到2.5%。150个核苷酸的VP1-2A连接区域内的所有替换都是同义的，而在其余VP1编码区域的31个可变位置中，多达8个位置在至少一个毒株中编码氨基酸替换。将可变氨基酸位置的可能结构定位映射到已发表的PV1/马奥尼结构模型上。大多数替换发生在已知或怀疑是中和抗体靶点的基序中的五重轴周围。我们认为，观察到的毒株之间显著的遗传差异是基于脊髓灰质炎病毒复制延长期间瓶颈传播事件和抗原漂移的综合作用。
