Infectivity and Shedding of Mouse Kidney Parvovirus After Oronasal Inoculation of C57BL/6, CD1, and NSG Mice.

IF 1.3 4区 农林科学 Q2 VETERINARY SCIENCES
Mandy L Kain, Rodolfo Ricart J Arbona, Kenneth S Henderson, Rajeev Dhawan, Sebastien Monette, Neil S Lipman
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引用次数: 0

Abstract

Mouse kidney parvovirus (MKPV), the etiology of murine inclusion body nephropathy, has been identified globally in mice used for research, with an estimated prevalence of 10% in academic colonies. In immunodeficient strains, MKPV causes significant morbidity and mortality, and severe renal pathology. In contrast, in immunocompetent mice, the infection is subclinical and causes minimal pathology. We investigated viral infectivity and shedding in inbred C57BL/6NCrl (B6), outbred Crl:CD1(ICR) (CD1), and highly immunocompromised NOD. Cg - Prkdc scid Il2rg tm1Wjl/SzJ (NSG) mice. Four doses, ranging from 1.16 × 10 3 to 1.16 × 10 6 viral copies per microliter, of an MKPV inoculum were administered oronasally to 3 mice per dose per mouse type. All 3 types (B6, CD1, and NSG) had persistent infection with prolonged shedding in urine and feces. Viral copy number in the urine generally increased over time, while shedding in the feces was more variable. Among the 3 populations, CD1 mice developed viral shedding in urine earliest (4 wk after inoculation) and at higher levels (greater than 1 × 10 7 viral copies per microliter). B6 mice become viruric later (7 wk after inoculation), with lesser virus shed (1 × 10 6 viral copies per microliter or less). In CD1 and B6 mice, peak urine shedding occurred at 11 to 14 wk after inoculation, after which levels gradually declined until 35 wk after inoculation (study endpoint). In contrast, NSG mice did not become viruric until 10 wk after inoculation and continued to shed large amounts of virus (greater than 1 × 107 viral copies per microliter) in urine until the study endpoint. Two commercial immunofluorescent serologic assays failed to detect serum antibodies to MKPV nonstructural protein 1 as late as 58 wk after inoculation, whereas immunohistochemistry of infected renal tissue successfully detected anti-MKPV serum antibodies. These results increase our knowledge of the biology of MKPV and have practical application for development of effective screening programs for this pathogen.

经口鼻接种C57BL/6、CD1和NSG小鼠肾细小病毒的传染性和脱落
小鼠肾细小病毒(MKPV)是小鼠包涵体肾病的病因,已在全球用于研究的小鼠中发现,在学术群体中估计患病率为10%。在免疫缺陷菌株中,MKPV引起显著的发病率和死亡率,以及严重的肾脏病理。相反,在免疫正常的小鼠中,感染是亚临床的,引起的病理很小。我们研究了近交的C57BL/6NCrl (B6)、近交的Crl:CD1(ICR) (CD1)和高度免疫低下的NOD的病毒感染和脱落。Cg - Prkdc scid Il2rg tm1Wjl/SzJ (NSG)小鼠。每微升1.16 × 10 3 ~ 1.16 × 10 6个病毒拷贝数范围内的MKPV接种物经口给药3只小鼠,每种小鼠类型每剂量。所有3种类型(B6、CD1和NSG)均持续感染,尿和粪便排出时间延长。尿液中的病毒拷贝数通常随着时间的推移而增加,而粪便中的病毒拷贝数则变化较大。在3个群体中,CD1小鼠在尿中出现病毒脱落最早(接种后4周),且水平较高(每微升病毒拷贝数大于1 × 10 7)。B6小鼠较晚(接种后7周)产生病毒,病毒脱落较少(每微升1 × 10 6个病毒拷贝或更少)。在CD1和B6小鼠中,尿量在接种后11至14周达到峰值,之后尿量逐渐下降,直到接种后35周(研究终点)。相比之下,NSG小鼠直到接种后10周才变为病毒,并继续在尿液中释放大量病毒(每微升大于1 × 107个病毒拷贝),直到研究结束。接种后58周,两种商业免疫荧光血清学检测都未能检测到MKPV非结构蛋白1的血清抗体,而感染肾组织的免疫组织化学检测则成功检测到抗MKPV血清抗体。这些结果增加了我们对MKPV生物学的认识,并对开发有效的该病原体筛选方案具有实际应用价值。
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来源期刊
Comparative medicine
Comparative medicine 医学-动物学
CiteScore
1.90
自引率
0.00%
发文量
71
审稿时长
6-12 weeks
期刊介绍: Comparative Medicine (CM), an international journal of comparative and experimental medicine, is the leading English-language publication in the field and is ranked by the Science Citation Index in the upper third of all scientific journals. The mission of CM is to disseminate high-quality, peer-reviewed information that expands biomedical knowledge and promotes human and animal health through the study of laboratory animal disease, animal models of disease, and basic biologic mechanisms related to disease in people and animals.
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