Horiuchi M, Yamaguchi Y, Gojobori T, Mochizuki M, Nagasawa H, Toyoda Y, Ishiguro N, Shinagawa M
Department of Veterinary Public Health, Research Center for Protozoan Molecular Immunology, Obihiro University of Agriculture and Veterinary Medicine, Inada-cho, Obihiro, Hokkaido, 080, Japan.
Virology. 1998 Sep 30;249(2):440-52. doi: 10.1006/viro.1998.9335.
Canine parvovirus (CPV) suddenly appeared in the late 1970s after which it showed continuous antigenic changes. Virological and molecular genetic analyses mainly focused on feline panleukopenia virus (FPLV) were conducted in this study because FPLV is the suspected ancestor of CPV; the way in which FPLV evolves may help to explain the emergence of CPV. Analysis of escape mutants against FPLV-specific monoclonal antibody showed that viruses possessing CPV-like properties were not easily detected in FPLV virus stocks. Phylogenetic analysis revealed that the nonstructural protein 1 (NS1) and capsid protein 2 (VP2) genes of FPLV changed with time. A similar tendency, however, was not observed in the FPLV VP2 proteins. In contrast, the topology of the phylogenetic tree of VP2 proteins of CPV basically concurred with that of the VP2 genes. Analysis of the ratio of nonsynonymous and synonymous substitutions revealed that synonymous substitutions exceeded nonsynonymous substitutions in both the NS1 and VP2 genes of FPLV, even when the analysis focused on specific regions in the VP2 gene that are known to be located on the capsid surface. Comparison of the CPV VP2 genes revealed that nonsynonymous substitution was found to dominate over synonymous substitution in one specific region in the VP2 gene. These results suggested that FPLV has changed mainly by random genetic drift. In contrast, after the appearance of CPV, changes in the CPV VP2 gene appear to be partly selected by certain positive selection forces. CPV and FPLV are known to be closely related viruses genetically and biologically, but the evolutionary mechanisms of the two viruses appeared to be different.
犬细小病毒（CPV）于20世纪70年代末突然出现，此后其抗原不断发生变化。本研究主要针对猫泛白细胞减少症病毒（FPLV）进行了病毒学和分子遗传学分析，因为FPLV被怀疑是CPV的祖先；FPLV的进化方式可能有助于解释CPV的出现。对针对FPLV特异性单克隆抗体的逃逸突变体分析表明，在FPLV病毒株中不容易检测到具有CPV样特性的病毒。系统发育分析表明，FPLV的非结构蛋白1（NS1）和衣壳蛋白2（VP2）基因随时间发生了变化。然而，在FPLV的VP2蛋白中未观察到类似趋势。相反，CPV的VP2蛋白系统发育树的拓扑结构与VP2基因的拓扑结构基本一致。对非同义替换与同义替换比例的分析表明，即使分析集中在VP2基因中已知位于衣壳表面的特定区域，FPLV的NS1和VP2基因中的同义替换也超过了非同义替换。对CPV VP2基因的比较表明，在VP2基因的一个特定区域中，非同义替换占主导地位。这些结果表明，FPLV主要通过随机遗传漂变发生变化。相比之下，CPV出现后，CPV VP基因的变化似乎部分受到某些正选择力的影响。已知CPV和FPLV在遗传和生物学上是密切相关的病毒，但这两种病毒的进化机制似乎不同。
