Abstract
Tissues from two cows with neurological signs that were admitted to the Vetsuisse Faculty under suspicion of rabies and bovine spongiform encephalopathy (BSE), respectively, were further analyzed for this case report. After histopathological examination and exclusion of BSE and rabies, the animals were diagnosed with etiologically unresolved disseminated non-suppurative encephalitis. Using next-generation sequencing, we detected the full genome of bovine polyomavirus 2 (BoPyV2) in brain samples from both animals. This virus has been identified in beef samples in three independent studies conducted in the United States and Germany, but has not been linked to any disease. Analysis of the two new BoPyV2 genome sequences revealed close phylogenetic relationships to one another and to BoPyV2 isolates detected in beef samples. In situ hybridization demonstrated the presence of viral nucleic acid in all investigated brain areas and in areas with signs of inflammation in both animals. Thus, we provide the first evidence that BoPyV2 is a probable cause of non-suppurative encephalitis in cattle, and encourage further molecular and serological testing to elucidate the disease’s epidemiology, as well as experimental transmission studies to prove causality between the infection and disease.
Highlights
Polyomavirus infections are often persistent and subclinical, but their potential to cause severe diseases in immunosuppressed humans is well known
We reported the identification of bovine polyomavirus 2 (BoPyV2) in a brain sample from a cow with encephalitis of unknown origin; we sequenced the full virus genome using next-generation sequencing (NGS) and confirmed the result with conventional polymerase chain reaction (PCR) [24]
Because the NGS data suggested a 45-bp insertion in the ORF of the large T antigen compared with closely related BoPyV2 sequences, this inconclusive region was Sanger sequenced and the insertion was revealed to be an alignment mistake
Summary
Polyomavirus infections are often persistent and subclinical, but their potential to cause severe diseases in immunosuppressed humans is well known. JC polyomavirus (JCPyV) and BK polyomavirus (BKPyV) are striking examples of viruses that become pathogenic in patients with AIDS and those under immunosuppressive treatment in the context of organ transplantation. Corresponding diseases, such as progressive multifocal leukoencephalopathy (PML), nephropathies, and hemorrhagic cystitis, often lead to fatal outcomes or transplant rejection, and play important roles in human medicine [1,2,3]. The Merkel cell polyomavirus (MCPyV), for instance, can induce high-grade skin carcinomas in immunosuppressed people by integrating its genome into the host genome [4].
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