Search bioRxiv⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2025.10.31.685885

IRIS PIGMENTATION IRREGULARITIES FOLLOWING AN AVIAN INFLUENZA OUTBREAK: IMPLICATIONS FOR DISEASE SURVEILLANCE AND POPULATION MONITORING IN A COLONIAL SEABIRD

Petalas, C.·Giacinti, J. A.·Provencher, J. F.·Rail, J.-F.·Avery-Gomm, S.·Lavoie, R.·Elliott, K. H.·Seyer, Y.
View original source ↗Export metadata ↓

Abstract

Emerging infectious diseases can have catastrophic impacts on wildlife populations, yet identifying individuals that survived exposure, especially when external symptoms are absent, remains challenging. Since 2021, a virulent strain of highly pathogenic avian influenza virus (HPAIV H5N1 clade 2.3.4.4b) has caused unprecedented mortality in wild birds across continents. Northern Gannets (Morus bassanus) are among the species that suffered significant population declines in Europe and North America. At North Americas largest gannet colony (Bonaventure Island) dramatic mortality and reproductive failure occurred in 2022. Following this event, researchers noted a subset of gannets displaying irregular iris pigmentation, raising the possibility that this visible change may indicate a lasting effect of infection. Here, we build on earlier observations linking irregular iris pigmentation to HPAIV exposure in gannets using anti-nucleoprotein (NP) and anti-hemagglutinin (H5) antibodies. This provides the first quantitative test of this relationship using serological data and field-based digital photography. Iris irregularities were strongly associated ({rho} = -0.72) with antibodies to NP, supporting the hypothesis that they can indicate past exposure. The likelihood of NP antibody detection increased with iris pigment irregularity--about 50% likelihood at 40% irregularity, 65% at 50%, 77% at 60%, and over 90% above 77% irregularity. Moderate correlations ({rho} = 0.30) were observed for H5 antibodies. Our findings provide quantitative support for the hypothesis that iris pigmentation irregularities may serve as a visible, non-invasive marker of past HPAIV exposure in gannets. If validated across colonies and years, iris assessment could offer a rapid tool for tracking population health and recovery following HPAIV outbreaks, enhancing conservation monitoring and disease surveillance. Lay SummaryOur research shows clear evidence that irregular iris pigmentation in Northern Gannets is strongly linked to past infection with a deadly bird flu strain. This visible marker could allow scientists to rapidly identify surviving birds and monitor population health after outbreaks, helping conservation efforts across affected colonies. HighlightsO_LIIris pigmentation irregularities reveal past avian influenza exposure. C_LIO_LIExtent of iris pigmentation irregularity correlates with antibody levels. C_LIO_LIExposure likelihood increases with degree of iris pigmentation irregularity. C_LIO_LICould provide a rapid, non-invasive tool for wildlife disease and conservation monitoring. C_LI Graphical abstracts O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=134 SRC="FIGDIR/small/685885v1_ufig1.gif" ALT="Figure 1"> View larger version (60K): org.highwire.dtl.DTLVardef@12fa683org.highwire.dtl.DTLVardef@15d23b1org.highwire.dtl.DTLVardef@1d2425eorg.highwire.dtl.DTLVardef@10367cd_HPS_FORMAT_FIGEXP M_FIG C_FIG

Explore related subjects

physiologyPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Petalas, C., Giacinti, J. A., Provencher, J. F., Rail, J.-F., Avery-Gomm, S., Lavoie, R., Elliott, K. H., Seyer, Y.. 2025-11-03. IRIS PIGMENTATION IRREGULARITIES FOLLOWING AN AVIAN INFLUENZA OUTBREAK: IMPLICATIONS FOR DISEASE SURVEILLANCE AND POPULATION MONITORING IN A COLONIAL SEABIRD. https://doi.org/10.1101/2025.10.31.685885

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

28S-rsRNA facilitates PASMC proliferation through PKM2 β-hydroxybutyrylation

Ribosomal RNA-derived small RNAs (rsRNAs) are nucleic acid fragments originating from rRNA, the functions and roles of which in diseases remain incompletely understood. We identified 28S rsRNA-CTC_L20, an rsRNA whose expression is upregulated in hypoxic pulmonary artery smooth muscle cells (PASMCs) and in lung tissues of pulmonary hypertension (PH) models. In hypoxic cells, 28S rsRNA-CTC_L20 promotes PASMC proliferation, and its knockdown mitigates SuHx-induced pulmonary hypertension and vascular remodeling. Mechanistically, 28S rsRNA-CTC_L20 modulates {beta}-hydroxybutyrate (BHB) production by maintaining the stability of ketogenic enzyme mRNAs through its "CTGNNGG" motif. Elevated levels of BHB enhance the {beta}-hydroxybutyrylation modification at K166 of pyruvate kinase M2 (PKM2), increasing its activity and driving glycolysis to sustain proliferation. These results link ketone body metabolism to glycolysis in hypoxic cells and define an rsRNA-BHB-PKM2 {beta}-hydroxybutyrylation axis in PH. They also point to 28S rsRNA-CTC_L20 as a potential target for treating vascular remodeling.

physiology↗
bioRxiv2026

Selective activation of estrogen receptors modulates electrical activity and insulin secretion in human EndoC-βH1 cells

Estrogen receptors (ERs), ER and ER{beta} have important roles in the physiology of the endocrine pancreas in animal models, but the effects of ER activation on insulin-secreting human cells are still poorly understood. Here, we investigated the role of ER and ER{beta} as modulators of electrical activity and insulin secretion in the insulin-secreting human cell line EndoC-{beta}H1. Immunocytochemical analysis revealed a widespread cellular distribution of ER, while ER{beta} was predominantly localized outside the nucleus. We observed that both estradiol (E2) and the ER{beta} agonist diarylpropionitrile (DPN) led to a decrease in insulin secretion in the absence of stimulatory glucose concentrations, without affecting insulin content. Patch-clamp experiments revealed that a 48-hour treatment with either the ER agonist PPT or DPN resulted in depolarization of the resting membrane potential, increased action potential firing frequency, and altered the action potential waveform in EndoC-{beta}H1 cells. PPT increased voltage-dependent Ca2+ channel currents, while DPN reduced K+ and Na+ currents. These results suggest that activation of ER and ER{beta} modulates beta-cell electrical activity through distinct pathways involving ion channels. The effects of E2, PPT, and DPN were not caused by altered expression levels of ion channel genes after 48 hours of treatment. This suggests that these receptors act extranuclearly without affecting gene expression. Together, our findings demonstrate that selective activation of ER and ER{beta} modulates beta-cell excitability through distinct electrophysiological mechanisms and that E2 and DPN reduce basal insulin secretion in human EndoC-{beta}H1 cells. These results support ER and ER{beta} as potential targets for modulating human pancreatic beta-cell function.

physiology↗
bioRxiv2026

Body weight modifies the efficacy of lifespan-extending interventions in ad libitum-fed mice

Geroprotective interventions are often assessed by extension of lifespan in ad libitum-fed mice. Increased lifespan could therefore reflect rescue of adverse phenotypes of unhealthy controls. We analysed body weight and survival for 33,780 mice in the Interventions Testing Program (ITP) to test whether treatment effects varied with body weight. In males, each added standard deviation of attained adult weight made treatment 6% more favourable (HR 0.94), more apparent for interventions that lowered body weight (HR 0.90). Median lifespan increase rose from 6.2% in mice in the lightest quartile to 20.2% in the heaviest pre-dosing weight quartile among those experiments, mainly because control survival declined more steeply with weight than that of the intervention group. The effect of body weight was consistent across 13 of 14 compounds and reflected weight attained during adulthood rather than in early life. Weight-dependence of intervention effects was weak in ITP females, possibly because median survival of controls exceeded that of every sampled non-ITP female control group. Amelioration of weight-associated risk is therefore implicated as a major contributor to lifespan increases relative to heavy, short-lived controls. The geroprotective effects of these interventions may thus be less apparent in metabolically healthier mice or humans.

physiology↗