Pedersen N C
Department of Medicine, School of Veterinary Medicine, University of California, Davis 95616.
Adv Exp Med Biol. 1987;218:529-50. doi: 10.1007/978-1-4684-1280-2_69.
A number of feline coronavirus isolates have been characterized over the last few years. These isolates consist of what we have referred to as feline enteric coronaviruses (FECVs) and feline infectious peritonitis viruses (FIPVs). FECVs cause a transient enteritis in kittens but no systemic illness. FIPVs, in contrast, cause a systemic and usually fatal disease syndrome characterized either by an exudative serositis or a disseminated granulomatous disease. Although the diseases they cause are quite different, FECVs and FIPVs are antigenically and morphologically indistinguishable from each other. FECVs have a strict tropism for mature intestinal epithelial cells and do not appear to replicate in macrophages. In contrast, FIPVs, appear to spread rapidly from the intestinal mucosa and replicate in macrophages. Experiments will be presented, and literature cited, that will allow us to make the following assumptions about the pathogenesis of FIPV infection: 1) FIPVs and FECVs represent a spectrum of viruses that differ only in infectivity (ability to evoke seroconversion following oral infection) and virulence (ability to cause FIP), 2) field isolates are generally nearer to FECVs in behavior than laboratory isolates made from animal passaged material, 3) immunity to FIPV appears to be of the premunition type and is maintained for as long as the infection persists in a reactivatable form, 4) strains of feline coronaviruses that do not cause systemic disease, such as FECVs or low virulence FIPVs, can actually sensitize cats to infection with virulent FIPV strains, 5) FeLV infection interferes with established FIP immunity and allows for the reactivation of disease in healthy carriers, 6) FIPV may be passaged from queen to kitten either in utero or during neonatal life, and 7) kittens infected by their mothers with FIPV do not usually develop FIP but become immune carriers of the virus for a period of 5-6 months; recovery from the carrier state is associated with a loss of premunition immunity.
在过去几年中,已经对一些猫冠状病毒分离株进行了特性鉴定。这些分离株包括我们所称的猫肠道冠状病毒(FECV)和猫传染性腹膜炎病毒(FIPV)。FECV在小猫中引起短暂性肠炎,但不会导致全身性疾病。相比之下,FIPV引起一种全身性且通常致命的疾病综合征,其特征为渗出性浆膜炎或播散性肉芽肿性疾病。尽管它们所引起的疾病截然不同,但FECV和FIPV在抗原性和形态学上彼此无法区分。FECV对成熟的肠上皮细胞具有严格的嗜性,似乎不在巨噬细胞中复制。相反,FIPV似乎从肠黏膜迅速扩散并在巨噬细胞中复制。将展示相关实验并引用文献,这将使我们能够对FIPV感染的发病机制做出以下假设:1)FIPV和FECV代表了一系列仅在感染性(口服感染后引起血清转化的能力)和毒力(引起FIP的能力)方面存在差异的病毒;2)野外分离株在行为上通常比从动物传代材料中获得的实验室分离株更接近FECV;3)对FIPV的免疫似乎属于带虫免疫类型,只要感染以可再激活的形式持续存在,免疫就会维持;4)不引起全身性疾病的猫冠状病毒株,如FECV或低毒力FIPV,实际上可使猫对强毒FIPV株的感染敏感;5)猫白血病病毒(FeLV)感染会干扰已建立的FIP免疫,并使健康携带者体内的疾病重新激活;6)FIPV可能在子宫内或新生儿期从母猫传给小猫;7)被母亲感染FIPV的小猫通常不会患上FIP,而是在5 - 6个月的时间内成为该病毒的免疫携带者;从携带状态恢复与带虫免疫的丧失有关。