Biology subjects

Boyle, D.

Publications and source records attributed to Boyle, D..

5 recordsLinked to original sources

bioRxiv2026

Migratory bird and marine mammal surveillance fails to find evidence for an HPAI H5N1 2.3.4.4b incursion into Australia in 2025

The panzootic caused by high pathogenicity avian influenza (HPAI) H5N1 clade 2.3.4.4b has been devastating for animals, globally. Despite global spread, the virus remains absent in Oceania. Herein we report the results of our fourth year of enhanced migratory bird surveillance, coinciding with the spring migration of wild birds in 2025; none of the 847 migratory wild birds or 38 marine mammals were positive for HPAI H5N1, although we did detect LPAI. Surveillance remains a critical tool for HPAI H5N1 response, with early detection and rapid response being critical to mitigate the impacts of this virus on animal, environment and human health.

microbiology↗

bioRxiv2025

Surveillance of migratory shorebirds and seabirds in 2024 in Australia reveals incursions of a diversity of low pathogenicity avian influenza viruses, but not high pathogenicity avian influenza H5N1

The current panzootic of high pathogenicity avian influenza (HPAI) H5N1 has been catastrophic for wildlife, and following a significant sweep, clade 2.3.4.4b is found in every region aside from Oceania. Herein, we report the results of our third year of targeted surveillance of incoming migratory seabirds and shorebirds into Australia. We did not find evidence of HPAI H5N1 in any of the birds tested, and there were no reports of HPAI H5N1 in wildlife tested through other surveillance schemes in 2024. Unlike previous years, we detected a diversity of low pathogenicity avian influenza (LPAI) viruses in shorebirds. Through phylogenetic analysis we revealed that the H3N7 and H4N7 viruses recovered from Red-necked Stints were complex mosaic viruses, comprising segments of Eurasian, Australian shorebird, and Australian waterfowl segments. A H1N7 virus detected comprised a wholly Eurasian introduction, confirming this route for avian influenza viruses into Australian ecosystems. These results provide further evidence for the key role of long-distance migratory shorebirds in introducing novel LPAI viruses into Oceania. While our focus on northern migration routes remained appropriate for HPAI H5N1 surveillance in 2024, the continued spread of HPAI H5N1 to sub-Antarctic Islands demands consideration of a potential southern incursion route for Oceania in future.

microbiology↗

bioRxiv2024

Long distance avian migrants fail to bring 2.3.4.4b HPAI H5N1 into Australia for a second year in a row

There is an ongoing and profound burden of lineage 2.3.4.4b high pathogenicity avian influenza (HPAI) H5N1 on wildlife and poultry, globally. Herein we report the continued absence of HPAI and antibodies against lineage 2.3.4.4b HPAI from October - December 2023, in migratory birds shortly after their arrival in Australia. Given the ever-changing phenotype of this virus, worldwide studies on the occurrence, or here absence of the virus, are of critical importance to understand the virus dispersal and incursion risk and development of response strategies.

microbiology↗

bioRxiv2024

Joint-specific rheumatoid arthritis fibroblast-like synoviocyte regulation identified by integration of chromatin access and transcriptional activity

The mechanisms responsible for the distribution and severity of joint involvement in rheumatoid arthritis (RA) are not known. To explore whether site-specific FLS biology might be associated with location-specific synovitis and explain the predilection for hand (wrist/metacarpal phalangeal joints) involvement in RA, we generated transcriptomic and chromatin accessibility data from FLS to identify the transcription factors (TFs) and pathways. Networks were constructed by integration of chromatin accessibility and gene expression data. Analysis revealed joint-specific patterns of FLS phenotype, with proliferative, migratory, proinflammatory, and matrix-degrading characteristics observed in resting FLS derived from the hand joints compared with hip or knee. TNF-stimulation amplified these differences, with greater enrichment of proinflammatory and proliferative genes in hand FLS compared with hip and knee FLS. Hand FLS also had the greatest expression of markers associated with an activated state relative to the resting state, with the greatest cytokine and MMP expression in TNF-stimulated hand FLS. Predicted differences in proliferation and migration were biologically validated with hand FLS exhibiting greater migration and cell growth than hip or knee FLS. Distinctive joint-specific FLS biology associated with a more aggressive inflammatory response might contribute to the distribution and severity of joint involvement in RA.

bioinformatics↗

bioRxiv2019

Platelet Thrombus Formation in eHUS is Prevented by Anti-MBL2

Epidemic Hemolytic Uremic Syndrome (eHUS) caused by Shiga toxin-producing bacteria is characterized by thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury that cause acute renal failure in up to 65% of affected patients. We hypothesized that the mannose-binding lectin (MBL) pathway of complement activation plays an important role in human eHUS, as we previously demonstrated that injection of Shiga Toxin-2 (Stx-2) led to fibrin deposition in mouse glomeruli that was blocked by co-injection of the anti-MBL-2 antibody 3F8. However, the markers of platelet thrombosis in affected mouse glomeruli were not delineated. To investigate the effect of 3F8 on markers of platelet thrombosis, we used kidney sections from our mouse model (MBL-2+/+ Mbl-A/C-/-; MBL2 KI mouse). Mice in the control group received PBS, while mice in a second group received Stx-2, and those in a third group received 3F8 and Stx-2. Using double immunofluorescence (IF) followed by digital image analysis, kidney sections were stained for fibrin(ogen) and CD41 (marker for platelets), von-Willebrand factor (marker for endothelial cells and platelets), and podocin (marker for podocytes). Electron microscopy (EM) was performed on ultrathin sections from mice and human with HUS. Injection of Stx-2 resulted in an increase of both fibrin and platelets in glomeruli, while administration of 3F8 with Stx-2 reduced both platelet and fibrin to control levels. EM studies confirmed that CD41-positive objects observed by IF were platelets. The increases in platelet number and fibrin levels by injection of Stx-2 are consistent with the generation of platelet-fibrin thrombi that were prevented by 3F8.

pathology↗