1Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts.
2CBSET, Inc., Lexington, Massachusetts.
Comp Med. 2024 Oct 31;74(5):344-351. doi: 10.30802/AALAS-CM-24-000015. Print 2024 Oct 1.
Mouse kidney parvovirus (MKPV) infection can cause significant morbidity and mortality by inducing moderate to severe inclusion body nephropathy and kidney fibrosis in aged immunodeficient mice. However, MKPV infection in immunocompetent mice is associated with histopathologic findings ranging from absent to minimal or moderate lymphoplasmacytic interstitial nephritis without inclusion body in most cases. We surveyed the prevalence of MKPV via PCR from August 2019 through January 2021, using feces, kidneys, and livers collected and pooled from 2 sentinel mice [Crl:CD1(ICR)] (CD1) per surveillance cage (a total of 212 cages). CD1 mice used as dirty-bedding sentinels were housed for 6 mo in a separate cage on the same rack as colony mice used in research at the Massachusetts Institute of Technology and at the Whitehead Institute for Biomedical Research. MKPV quantitative PCR positivity was 16.04%, 14.62%, and 10.02% for feces, kidney, and liver, respectively. The aggregate prevalence of MKPV was 22.64% (48 of 212 samples). Thirty-three of 103 rooms (32.04%) were MKPV positive. MKPV-positive kidneys had more severe chronic lymphoplasmacytic interstitial nephritis (CLIN) than MKPV-negative kidneys; however, there was no significant difference in hepatic lesions between MKPV-positive and -negative livers. Although no overt intranuclear inclusion body nephropathy was noted in MKPV-positive CD1 kidneys, MKPV RNA was sporadically detected within tubular epithelial cells in MKPV-positive kidneys but not in MKPV-positive livers. Our study indicates that MKPV can be easily transmitted through soiled bedding. It highlights that CD1 mice can be used as sentinels to detect MKPV, emphasizing the importance of monitoring MKPV distribution using quantitative PCR in sentinel mice if MKPV needs to be excluded from a colony. Importantly, as MKPV infection is associated with mild to moderate CLIN, MKPV can potentially confound the interpretation of in vivo biomedical data.
鼠肾细小病毒(MKPV)感染可引起中度至重度包涵体肾病和纤维化,导致老年免疫缺陷小鼠发病率和死亡率显著升高。然而,免疫功能正常的小鼠感染 MKPV 时,大多数情况下组织病理学表现为从无到轻微或中度淋巴浆细胞性间质性肾炎,无包涵体。我们通过聚合酶链反应(PCR),从 2019 年 8 月至 2021 年 1 月,对 212 个监测笼(每个监测笼 2 只哨兵鼠 [Crl:CD1(ICR)] [CD1])收集的粪便、肾脏和肝脏进行了 MKPV 检测。作为脏垫哨兵的 CD1 小鼠被单独饲养在与麻省理工学院和怀特海德生物医学研究所用于研究的群体小鼠相同的架子上的笼子中 6 个月。粪便、肾脏和肝脏的 MKPV 定量 PCR 阳性率分别为 16.04%、14.62%和 10.02%。MKPV 的总流行率为 22.64%(48/212 个样本)。33/103 个房间(32.04%)MKPV 阳性。MKPV 阳性肾脏的慢性淋巴浆细胞性间质性肾炎(CLIN)比 MKPV 阴性肾脏更严重;然而,MKPV 阳性和阴性肝脏的肝损伤无显著差异。虽然在 MKPV 阳性 CD1 肾脏中未观察到明显的核内包涵体肾病,但在 MKPV 阳性肾脏的肾小管上皮细胞中偶尔检测到 MKPV RNA,但在 MKPV 阳性肝脏中未检测到。我们的研究表明,MKPV 可以通过污染的垫料轻易传播。它强调了 CD1 小鼠可用作哨兵来检测 MKPV,强调如果需要从群体中排除 MKPV,则使用定量 PCR 在哨兵小鼠中监测 MKPV 分布的重要性。重要的是,由于 MKPV 感染与轻度至中度 CLIN 相关,因此 MKPV 可能会影响体内生物医学数据的解释。