WNS fungus increases replication of bat coronavirus

In recent years, viruses found in bats are thought to have spilled over to humans and other mammals, causing fatal disease. These spill-overs appear to be associated with increased contact between bats and other animals as well as increased shedding of virus by bats. Here, we tested the prediction that little brown bats (Myotis lucifugus) co-infected with the M. lucifugus coronavirus (Myl-CoV) and with Pseudogymnoascus destructans, the fungus that causes bat white-nose syndrome (WNS) exhibit different disease severity, viral shedding and molecular responses than singly-infected or mock-infected bats. We recently showed that > 30% of these bats were infected with the Myl-CoV, and there was no difference in prevalence of the virus between the WNS- and mock-infected bats. Here, we show that the intestines of virus-infected bats co-infected with WNS contained on average 60-fold more viral RNA than singly-infected bats. Increased viral RNA correlated with the severity of WNS-related pathology, and the intestines of bats with WNS contained lower levels of interleukin-22 receptor (IL-22 RA1), and higher levels of chemokine ligand 25 (CCL25) and Ras-like estrogen-regulated growth inhibitor (RERG). Levels of coronavirus antibodies were higher in WNS-infected bats when compared with mock-infected bats. Our results suggest that the systemic effects of WNS may down-regulate anti-viral responses in persistently infected M. lucifugus and increase the potential of virus shedding.