Bullock, J.; Bulloch, B.; Wickenhagen, A.; Gallogly, S.; Kaiser, F.; Schulz, J. E.; Bushmaker, T.; Koolaparambil Mukesh, R.; Williamson, B. N.; Hawes, K.; McBain, A.; Prado-Smith, J.; Clancy, C. S.; Smith, B. J.; Port, J. R.; de Wit, E.; van Tol, S.

Henipaviruses (HNV), Hendra (HeV) and Nipah (NiV) virus, cause severe pulmonary and neurologic disease in humans and other mammals. Bats in the genus Pteropus naturally host HeV and NiV, but their feasibility in experimental studies is limited due to their large size, low fertility rate, and unavailability outside of their native range. Understanding bat-henipavirus interactions that regulate shedding and replication could improve mitigation of spillover events and illuminate the factors that differentiate severe and controlled HNV infection. Here, we assessed the suitability of the Jamaican fruit bat (JFB) (Artibeus jamaicensis) to model HNV infection in vitro and in vivo. JFB primary kidney cells were permissive to HNVs, and HeV and NiV antagonized the induction of the innate antiviral response. JFBs were inoculated via the intranasal and oral routes (IN/PO) with HeV or NiV or intravenously (IV) with HeV and monitored for 7 days. Following IN/PO exposure, infection was quenched rapidly and limited HeV RNA was detected in oral swabs and tissues while NiV RNA was found in only one oral swab. HeV IV inoculation resulted in robust, disseminated infection and viral RNA was detected in oral, rectal, and environmental swabs. Overall, these results support that JFBs are susceptible to both viruses, but replication is quenched rapidly in vivo following IN/PO exposure. Future studies will optimize the in vivo model to leverage the JFB to further our understanding of bat-henipavirus interactions.