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Bulloch, B.

Publications and source records attributed to Bulloch, B..

3 recordsLinked to original sources
bioRxiv2026

A Synthetic Consensus Chiroptera IFN-β Induces IFN-I Signaling Across Diverse Bat Taxa

Bat-associated viruses consistently spill over from bats into humans and other animals. Many bat-associated viruses, including Marburg virus and Nipah virus, cause severe disease in humans but their presentation is subclinical in bats. Advancements in tools and resources to study bat innate antiviral immune responses, including the type I IFN (IFN-I) pathway, are needed to evaluate the mechanisms that underlie differential infection outcomes between reservoir bats and spillover hosts. Commercially available IFN-Is are not bat-specific, and conspecific IFN-Is are impractical to produce for the over 1,500 described bat species. Here, we design and validate a bat order-level consensus IFN (Chiroptera IFN-{beta}) that is functional in bat cells from six diverse bat families, including representatives from both suborders. Using Jamaican fruit bat cells, we demonstrate that Chiroptera IFN-{beta} induces an IFN-stimulated gene repertoire comparable to conspecific IFN-{beta}. This valuable resource can accelerate the capacity of the field to study bat innate antiviral responses and illuminate differences between bats and humans.

immunology↗
bioRxiv2026

Jamaican fruit bats are susceptible to henipaviruses but rapidly control infection

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. Author SummaryHenipaviruses (HNV) spillover from pteropid bat species and cause severe diseases in humans. Many gaps limit our understanding of HNV-bat interactions that influence spillover and effective control of infection. Here, we evaluate the Jamaican fruit bat (JFB) as a henipavirus model. We demonstrate that JFB cells are permissive all HNVs evaluated, and that JFBs support Hendra virus replication and shedding without signs of clinical disease.

microbiology↗