Center for Companion Animal Health, School of Veterinary Medicine, University of California, One Shields Avenue, Davis, CA, 95616, USA; E-mail:
Viruses. 2009 Sep;1(2):166-84. doi: 10.3390/v1020166. Epub 2009 Aug 26.
The internal FECV→FIPV mutation theory and three of its correlates were tested in four sibs/half-sib kittens, a healthy contact cat, and in four unrelated cats that died of FIP at geographically disparate regions. Coronavirus from feces and extraintestinal FIP lesions from the same cat were always >99% related in accessory and structural gene sequences. SNPs and deletions causing a truncation of the 3c gene product were found in almost all isolates from the diseased tissues of the eight cats suffering from FIP, whereas most, but not all fecal isolates from these same cats had intact 3c genes. Other accessory and structural genes appeared normal in both fecal and lesional viruses. Deliterious mutations in the 3c gene were unique to each cat, indicating that they did not originate in one cat and were subsequently passed horizontally to the others. Compartmentalization of the parental and mutant forms was not absolute; virus of lesional type was sometimes found in feces of affected cats and virus identical to fecal type was occasionally identified in diseased tissues. Although 3c gene mutants in this study were not horizontally transmitted, the parental fecal virus was readily transmitted by contact from a cat that died of FIP to its housemate. There was a high rate of mutability in all structural and accessory genes both within and between cats, leading to minor genetic variants. More than one variant could be identified in both diseased tissues and feces of the same cat. Laboratory cats inoculated with a mixture of two closely related variants from the same FIP cat developed disease from one or the other variant, but not both. Significant genetic drift existed between isolates from geographically distinct regions of the Western US.
内部 FECV→FIPV 突变理论及其三个相关理论在四只同窝/半同窝小猫、一只健康接触猫以及四只在地理上不同地区死于 FIP 的无关猫中进行了测试。来自同一猫粪便和肠外 FIP 病变的冠状病毒在辅助和结构基因序列上总是 >99%相关。在患有 FIP 的八只猫的病变组织中几乎所有分离株中都发现了导致 3c 基因产物截断的 SNP 和缺失，而大多数（但不是全部）来自这些相同猫的粪便分离株具有完整的 3c 基因。其他辅助和结构基因在粪便和病变病毒中均正常。3c 基因中的有害突变在每只猫中都是独特的，表明它们不是从一只猫起源，然后横向传播给其他猫。亲本和突变形式的分隔并不是绝对的；病变型病毒有时在受感染猫的粪便中发现，而与粪便型相同的病毒偶尔在病变组织中鉴定出。尽管本研究中的 3c 基因突变没有横向传播，但从死于 FIP 的猫传播给其同屋室友的亲本粪便病毒很容易传播。所有结构和辅助基因在猫体内和猫之间都具有很高的变异性，导致微小的遗传变异。在同一猫的病变组织和粪便中都可以识别出一种以上的变异。用来自同一 FIP 猫的两种密切相关变体的混合物接种的实验猫会从一种或另一种变体中发病，但不会同时发病。来自美国西部不同地理区域的分离株之间存在显著的遗传漂移。
