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从感染猫肠道冠状病毒的免疫功能低下的猫中分离出的两种相关的猫传染性腹膜炎病毒毒株。

Two related strains of feline infectious peritonitis virus isolated from immunocompromised cats infected with a feline enteric coronavirus.

作者信息

Poland A M, Vennema H, Foley J E, Pedersen N C

机构信息

Center for Companion Animal Health, School of Veterinary Medicine, University of California, Davis 95616, USA.

出版信息

J Clin Microbiol. 1996 Dec;34(12):3180-4. doi: 10.1128/jcm.34.12.3180-3184.1996.

Abstract

Two groups of cats were experimentally infected orally with the cat-passaged RM strain of feline enteric coronavirus (FECV-RM). One group of cats (n = 19) had been chronically infected with feline immunodeficiency virus (FIV) for over 6 years, while a second control group (n = 20) consisted of FIV-naive siblings. Fecal virus shedding of FECV occurred in both groups starting on day 3 postinfection, nearly ceased by 4 weeks in FIV-uninfected cats, but remained at high levels in FIV-infected animals. FIV-infected cats shed virus for a longer period of time and at levels 10 to 100 times greater than those for FIV-uninfected cats. The coronavirus antibody response of the FIV-infected cats was delayed and of reduced titer compared with that of the FIV-uninfected animals. Cats in both groups remained asymptomatic for the first two months following FECV-RM infection; however, 8 to 10 weeks postinfection two cats in the FIV-infected group developed feline infectious peritonitis (FIP). The FIP viruses (designated FIPV-UCD9 and -UCD10) isolated from these two cats had almost complete genetic homology to each other and to the infecting FECV-RM. However, unlike FECV-RM, they readily induced FIP when inoculated intraperitoneally into specific-pathogen-free cats. This study confirms that FIPVs are frequently and rapidly arising mutants of FECV. Immunosuppression caused by chronic FIV infection may have enhanced the creation and selection of FIPV mutants by increasing the rate of FECV replication in the bowel and inhibiting the host's ability to combat the mutant viruses once they occurred.

摘要

将两组猫通过口服途径用猫肠道冠状病毒的猫传代RM株(FECV-RM)进行实验性感染。一组猫(n = 19)已感染猫免疫缺陷病毒(FIV)达6年以上,而另一对照组(n = 20)由未感染FIV的同胞猫组成。两组猫在感染后第3天开始出现FECV粪便病毒排出,在未感染FIV的猫中,到4周时几乎停止,但在感染FIV的动物中仍维持在高水平。感染FIV的猫排出病毒的时间更长,排出水平比未感染FIV的猫高10至100倍。与未感染FIV的动物相比,感染FIV的猫的冠状病毒抗体反应延迟且滴度降低。两组猫在感染FECV-RM后的头两个月均无症状;然而,感染后8至10周,感染FIV组的两只猫发生了猫传染性腹膜炎(FIP)。从这两只猫中分离出的FIP病毒(命名为FIPV-UCD9和-UCD10)彼此之间以及与感染的FECV-RM几乎具有完全的基因同源性。然而,与FECV-RM不同,当将它们腹腔内接种到无特定病原体的猫中时,它们很容易诱发FIP。这项研究证实FIPV是FECV频繁且快速产生的突变体。慢性FIV感染引起的免疫抑制可能通过增加FECV在肠道中的复制速率并抑制宿主一旦出现突变病毒后对抗突变病毒的能力,从而增强了FIPV突变体的产生和选择。

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