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An atypical parvovirus driving chronic tubulointerstitial nephropathy and kidney fibrosis

ABSTRACT: We have performed RNA sequencing on kidneys from inclusion body nephropathy-affected mice and compared the data to healthy, uninfected controls. Using a metagenomics approach, we report the identification of the disease causing agent as an atypical virus, mouse kidney parvovirus (MKPV), belonging to a divergent genus of the Parvoviridae. The RNA sequencing also enabled us to assess the host response to MKPV-infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE117710 | GEO | 2018/07/27

REPOSITORIES: GEO

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An atypical parvovirus driving chronic tubulointerstitial nephropathy and kidney fibrosis

Project description:The occurrence of a spontaneous nephropathy in laboratory mice, characterized by tubular degeneration and intranuclear inclusions, has puzzled pathologists for over four decades. While the condition takes a more severe course in immunodeficient animals suggesting an infectious cause, its etiology has remained elusive. Using an unbiased metagenomics approach, we have identified the causative agent as a novel virus, mouse kidney parvovirus (MKPV), belonging to a divergent and unclassified genus of the Parvoviridae. MKPV was found to be present in animal facilities in Australia and North America, is transmitted via the orofecal route and is controlled by the adaptive immune system. Detailed analysis of the clinical course and histopathologic features demonstrated a stepwise progression of pathology ranging from sporadic tubular inclusions to extensive tubular degeneration and interstitial fibrosis culminating in renal failure. In summary, we identify a novel, widely distributed pathogen in laboratory mice causing significant impact on the interpretation and outcome of biomedical research based on mouse models. Additionally, we establish MKPV-induced nephropathy as a new tool for elucidating the mechanisms of tubulointerstitial fibrosis that shares molecular features with chronic kidney disease in humans.

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