CHARACTERIZATION OF A CORONAVIRUS FROM RABBITS

我们的目的是研究兔冠状病毒(RbCV)的致病机理。 兔对这种病毒的生理反应，以及与 Rbcv传给冠状病毒科其他成员。血清中和研究 用犬冠状病毒(CCV)抗血清抗RbCV，猫传染性 腹膜炎(FIP)和传染性胃肠炎(TGE)病毒 完好无损的兔完成。结果：CCV 2/3，FIP 2/3，TGE 1/3， Rbcv 3/3存活。仅Rbcv一项就是致命的。所有接受RbCV的兔 与包括RbCV在内的一种冠状病毒的抗血清结合 出现了疾病的临床症状。正如预期的那样，RbCV抗血清静音 临床症状最多。RbCV与CCV、FIP或TGE抗血清反应 制作了一张疾病的典型临床图景。在一些幸存者身上， 直肠温度在10-12天内保持在40摄氏度以上，其他 体温模式与接受RbCV+的兔的体温模式相似 RbCV抗血清。那些死亡的人的大体损伤类似于兔子 孤身一人死于RbCV。在死亡的幸存者中没有观察到大体损害 在康复之后。基于之前的工作，显示了双向杂交 冠状病毒229E(人)，部分交叉保护接种疫苗 CCV和FIP，而这一新数据，RbCV最有可能属于 冠状病毒科。需要进行核苷酸同源性研究来证明这一点。 假设。肌酸激酶测定对心肌损伤的评估 同工酶正在进行中。将进一步尝试使RbCV适应 组织培养。这项工作的意义在于学习的能力 一种病毒性疾病，在一种动物身上有嗜心性，但 规模可控，允许按顺序进行临床和生理操作 观察。RbCV对兔心脏的损害有一定的推论 携带柯萨奇病毒的人心脏，肺炎支原体， 流感病毒、带状疱疹，可能还有其他感染源。

Our objective is to study the pathogenesis of rabbit coronavirus (RbCV), the rabbit's physiologic response to this virus, and the relatedness of RbCV to other members of the Coronaviridae. Serum neutralization studies against RbCV with antiserum to canine coronavirus (CCV), feline infectious peritonitis (FIP), and transmissible gastroenteritis (TGE) viruses in the intact rabbit were completed. Results were: CCV 2/3, FIP 2/3, TGE 1/3, RbCV 3/3 survived. RbCV alone was lethal. All rabbits receiving RbCV in combination with antiserum to one of the coronaviruses, including RbCV showed clinical signs of disease. As expected RbCV antiserum muted clinical signs the most. RbCV reacted with antisera to CCV, FIP, or TGE produced a typical clinical picture of disease. In some survivors the rectal temperature remained above 40 degrees C for 10-12 days and in others the temperature pattern closely followed that of rabbits receiving RbCV + RbCV antiserum. Gross lesions in those which died were similar to rabbits dying with RbCV alone. Gross lesions were not observed in survivors killed following recovery. Based on previous work showing a 2 way cross with coronavirus 229E (Human), partial cross protection from vaccination with CCV and FIP, and this new data, RbCV is most probably in Group II of the Coronaviridae. Nucleotide homology studies will be required to prove this supposition. Assessment of myocardial damage measuring creatine kinase isozymes are in progress. Further attempts will be made to adapt RbCV to tissue culture. The significance of this work lies in the ability to study a viral disease with a cardiotropism in an animal of sufficient but manageable size to allow sequential clinical and physiological observations. The damage to the rabbit heart by RbCV has a corollary in the human heart with the Coxsackie viruses, Mycoplasma pneumoniae, influenza virus, Herpes zoster, and possibly other infectious agents.