Pedersen Niels C, Liu Hongwei, Gandolfi Barbara, Lyons Leslie A
Center for Companion Animal Health, School of Veterinary Medicine, University of California-Davis, One Shields Avenue, Davis, CA 95616, USA.
Center for Companion Animal Health, School of Veterinary Medicine, University of California-Davis, One Shields Avenue, Davis, CA 95616, USA.
Vet Immunol Immunopathol. 2014 Nov 15;162(1-2):33-40. doi: 10.1016/j.vetimm.2014.09.001. Epub 2014 Sep 16.
Naturally occurring feline infectious peritonitis (FIP) is usually fatal, giving the impression that immunity to the FIP virus (FIPV) is extremely poor. This impression may be incorrect, because not all cats experimentally exposed to FIPV develop FIP. There is also a belief that the incidence of FIP may be affected by a number of host, virus, and environmental cofactors. However, the contribution of these cofactors to immunity and disease incidence has not been determined. The present study followed 111 random-bred specific pathogen free (SPF) cats that were obtained from a single research breeding colony and experimentally infected with FIPV. The cats were from several studies conducted over the past 5 years, and as a result, some of them had prior exposure to feline enteric coronavirus (FECV) or avirulent FIPVs. The cats were housed under optimized conditions of nutrition, husbandry, and quarantine to eliminate most of the cofactors implicated in FIPV infection outcome and were uniformly challenge exposed to the same field strain of serotype 1 FIPV. Forty of the 111 (36%) cats survived their initial challenge exposure to a Type I cat-passaged field strains of FIPV. Six of these 40 survivors succumbed to FIP to a second or third challenge exposure, suggesting that immunity was not always sustained. Exposure to non-FIP-inducing feline coronaviruses prior to challenge with virulent FIPV did not significantly affect FIP incidence but did accelerate the disease course in some cats. There were no significant differences in FIP incidence between males and females, but resistance increased significantly between 6 months and 1 or more years of age. Genetic testing was done on 107 of the 111 infected cats. Multidimensional scaling (MDS) segregated the 107 cats into three distinct families based primarily on a common sire(s), and resistant and susceptible cats were equally distributed within each family. Genome-wide association studies (GWAS) on 73 cats that died of FIP after one or more exposures (cases) and 34 cats that survived (controls) demonstrated four significant associations after 100k permutations. When these same cats were analyzed using a sib-pair transmission test, three of the four associations were confirmed although not with genome-wide significance. GWAS was then done on three different age groups of cases to take into account age-related resistance, and different associations were observed. The only common and strong association identified between the various GWAS case configurations was for the 34.7-45.8Mb region of chromosome A3. No obvious candidate genes were present in this region.
自然发生的猫传染性腹膜炎(FIP)通常是致命的,这给人一种印象,即对FIP病毒(FIPV)的免疫力极差。这种印象可能是错误的,因为并非所有实验性接触FIPV的猫都会患上FIP。也有人认为FIP的发病率可能受多种宿主、病毒和环境辅助因素的影响。然而,这些辅助因素对免疫和疾病发病率的作用尚未确定。本研究跟踪了111只从单一研究繁殖群体获得的随机繁殖的无特定病原体(SPF)猫,并对它们进行了FIPV实验性感染。这些猫来自过去5年进行的几项研究,因此,其中一些猫先前接触过猫肠道冠状病毒(FECV)或无毒力的FIPV。这些猫被饲养在营养、饲养管理和隔离的优化条件下,以消除大多数与FIPV感染结果相关的辅助因素,并统一用同一血清型1的FIPV野外毒株进行攻击暴露。111只猫中有40只(36%)在首次接触I型猫传代FIPV野外毒株的攻击暴露中存活下来。这40只幸存者中有6只在第二次或第三次攻击暴露时死于FIP,这表明免疫力并非总能持续。在用强毒FIPV攻击之前接触非FIP诱导性猫冠状病毒对FIP发病率没有显著影响,但在一些猫中确实加速了病程。雄性和雌性之间的FIP发病率没有显著差异,但6个月至1岁或以上的猫的抵抗力显著增强。对111只受感染猫中的107只进行了基因检测。多维标度分析(MDS)主要根据共同的父系将107只猫分为三个不同的家族,抗性和易感猫在每个家族中分布均匀。对73只在一次或多次暴露后死于FIP的猫(病例)和34只存活的猫(对照)进行全基因组关联研究(GWAS),在100k次置换后显示出四个显著关联。当使用同胞对传递测试分析这些相同的猫时,四个关联中的三个得到了证实,尽管没有达到全基因组显著性。然后对三个不同年龄组的病例进行GWAS,以考虑与年龄相关的抗性,并观察到了不同的关联。在各种GWAS病例配置之间确定的唯一常见且强关联是在A3染色体的34.7 - 45.8Mb区域。该区域没有明显的候选基因。