Biology subjects

Bullock, J.

Publications and source records attributed to Bullock, J..

3 recordsLinked to original sources

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↗

bioRxiv2023

A model of sediment retention by vegetation for Great Britain: new methodologies & validation

Soil erosion is an substantial environmental concern worldwide. It has been historically and is of increasingly concern currently. Next to natural processes, over 2 million hectares of soil are at risk of erosion through intensifying agriculture in the Great Britain (England, Wales, Scotland and their territorial islands). Predictive soil erosion models, in the form of Ecosystem Service tools, aid in helping to identify areas that are vulnerable to soil erosion. Yet, no predictions for erosion or sediment retention by vegetation based on local data have been developed for Great Britain or the United Kingdom as a whole. Here we develop an erosion retention model using the InVEST platform, which is based on the RUSLE mathematical framework. We parameterise the model, as far as feasible, with GB specific input data. The developed model estimations are validated against suspended solids concentrations (sediments) in throughout England and Wales. Next to presenting the first GB wide estimate of erosion and erosion retention using the InVEST SDR module, we test three approaches here that differ from more widely applicable RUSLE model inputs, such as created for Europe as a whole. Here, we incorporate (1) periodicity to allow erosion to potentially fluctuate within years; (2) GB-specific cover periodic management factors estimates, including a range of crop types, based on observed satellite NDVI values (3) soil erosivity under heavy rainfall following GB estimates for 2000-2019. We conclude that both the GB created erosivity layer as the added periodicity do not seem to be provide substantial improvement over non-periodic estimated created with more widely available data, when validated against this set of suspended solids in rivers. In contrast, the observed cover management factors calculated from NDVI are a good improvement affecting the ranking order among catchments. Therefore, the generating of cover management factors using NDVI data could be promoted as method for InVEST SDR model development and in more general for developing RUSLE-based erosion estimates worldwide.

bioinformatics↗

bioRxiv2021

Degradation of Photoreceptor Outer Segments by the Retinal Pigment Epithelium Requires Pigment Epithelium-derived Factor Receptor (PEDF-R)

PurposeTo examine the contribution of PEDF-R to the phagocytosis process. Previously, we identified PEDF-R, the protein encoded by the PNPLA2 gene, as a phospholipase A2 in the retinal pigment epithelium (RPE). During phagocytosis, RPE cells ingest abundant phospholipids and protein in the form of photoreceptor outer segment (POS) tips, which are then hydrolyzed. The role of PEDF-R in RPE phagocytosis is not known. MethodsMice in which PNPLA2 was conditionally knocked out in the RPE were generated (cKO). Mouse RPE/choroid explants were cultured. Human ARPE-19 cells were transfected with siPNPLA2 silencing duplexes. POS were isolated from bovine retinas. The phospholipase A2 inhibitor bromoenol lactone was used. Transmission electron microscopy, immunofluorescence, lipid labeling, pulse-chase experiments, western blots, and free fatty acid and {beta}-hydroxybutyrate assays were performed. ResultsThe RPE of the cKO mice accumulated lipids as well as more abundant and larger rhodopsin particles compared to littermate controls. Upon POS exposure, RPE explants from cKO mice released less {beta}-hydroxybutyrate compared to controls. After POS ingestion during phagocytosis, rhodopsin degradation was stalled both in cells treated with bromoenol lactone and in PNPLA2-knocked-down cells relative to their corresponding controls. Phospholipase A2 inhibition lowered {beta}-hydroxybutyrate release from phagocytic RPE cells. PNPLA2 knock down also resulted in a decline in fatty acids and {beta}-hydroxybutyrate release from phagocytic RPE cells. ConclusionsPEDF-R downregulation delayed POS digestion during phagocytosis. The findings imply that efficiency of RPE phagocytosis depends on PEDF-R, thus identifying a novel contribution of this protein to POS degradation in the RPE.

biochemistry↗