Exposure to raccoon polyomavirus (RacPyV) in free-ranging North American raccoons (Procyon lotor)

Abstract

There is evidence that raccoon polyomavirus is causative for neuroglial brain tumors in the western United States. It is unknown if infection is limited to geographic locales where tumors have been reported or is widespread, like human polyomaviruses. We demonstrate raccoons in western, eastern and midwestern states have been exposed to RacPyV by detection of antibodies to capsid protein, VP1. While raccoons in eastern and midwestern states are seropositive, exposure is lower than in the western states. Additionally, across geographic areas seropositivity is higher in older compared to younger raccoons, similar to polyomavirus exposure in humans. Serum titers are significantly higher in raccoons with tumors compared to raccoons without. Unlike polyomavirus-associated diseases in humans, we did not detect significant sequence variation between tumor and non-tumor tissue in raccoons with tumors compared to those without tumors. This warrants further investigation into co-morbid diseases or genetic susceptibility studies of the host.

Procyonidae, Viverridae, Hyenidae, Herpestidae, Eupleridae, and Prionodontidae

“…This suggests RacPyV as having an important role in the promotion of neoplasia in neural stem cells. Serological surveys have confirmed viral exposure in free-ranging raccoons with and without tumors across the United States and Canada with, suggesting additional factors may play a role in the oncogenesis of these tumors (Church et al, 2016b).…”

BRD4 is associated with raccoon polyomavirus genome and mediates viral gene transcription and maintenance of a stem cell state in neuroglial tumour cells

“…This wide tissue distribution and low viral quantity is consistent with persistent polyomaviral infections (Bialasiewicz et al, 2009;Chesters et al, 1983;Dubensky & Villarreal, 1984;Sadeghi et al, 2014). Raccoon neuroglial brain tumour tissue contains high viral copies that are not associated with genetic mutation or insertion into the host cell genome (Dela Cruz et al, 2013;Church et al, 2016). This is in contrast to human polyomaviruses, in which disease-specific genotypes (JC polyomaviruses) or partial loss of viral genome associated with integration (Merkel cell polyomavirus) is identified (Gosert et al, 2010;Feng et al, 2008).…”

Identification of a Second Raccoon-Associated Polyomavirus

“…Serologic testing indicates that wild raccoons in the eastern United States have antibodies that bind the VP1 major capsid protein of RacPyV1 (4). We attempted to isolate and sequence the RacPyV1-like virus that presumably infects raccoons in Georgia.…”