Murine and related chapparvoviruses are nephro-tropic and produce novel accessory proteins in infected kidneys
Quintin Lee, Matthew P. Padula, Natalia Pinello, Simon H. Williams, Matthew B. O’Rourke, Marcílio Jorge Fumagalli, Joseph D. Orkin, Renhua Song, Babak Shaban, Ori Brenner, John E. Pimanda, Wolfgang Weninger, William Marciel de Souza, Amanda Melin, Justin Wong, Marcus J Crim, Sébastien Monette, Ben Roediger, Christopher J. Jolly
Abstract
Mouse kidney parvovirus (MKPV) is a member of the provisional genus Chapparvovirus that causes renal disease in immune-compromised mice, with a disease course reminiscent of polyomavirus-associated nephropathy in immune-suppressed kidney transplant patients. Here we map four major MKPV transcripts, created by alternative splicing, to a common initiator region, and use mass spectrometry to identify "p10" and "p15" as novel chapparvovirus accessory proteins produced in MKPV-infected kidneys. p15 and the splicing-dependent putative accessory protein NS2 are conserved in all near-complete amniote chapparvovirus genomes currently available (from mammals, birds and a reptile). In contrast, p10 may be encoded only by viruses with >60% amino acid identity to MKPV. We show that MKPV is kidney-tropic and that the bat chapparvovirus DrPV-1 and a non-human primate chapparvovirus, CKPV, are also found in the kidneys of their hosts. We propose, therefore, that many mammal chapparvoviruses are likely to be nephrotropic.