Biology subjects

Herrmann, C.

Publications and source records attributed to Herrmann, C..

At least 19 recordsLinked to original sources

bioRxiv2026

Effect of stimulation parameters for transcranial temporal interference stimulation to enhance occipital alpha-oscillations in healthy participants

Transcranial temporal interference stimulation (tTIS) has recently emerged as a non-invasive method for modulating neural activity using interfering high-frequency electric fields. Although behavioral and neuroimaging effects of tTIS have been reported, evidence for electrophysiological modulation remains inconsistent, and it is unclear whether observed effects are attributable to temporal interference itself or to other components of the signal, e.g. high-frequency carrier signals. We therefore investigated whether tTIS at to the individual alpha frequency (IAF) modulates occipital alpha power compared with both sham stimulation and an active high-frequency carrier control. Eighteen healthy participants were enrolled in a randomized, double-blind, within-subject crossover study; 17 participants were included in the final analysis. Each participant completed three stimulation sessions consisting of three conditions (tTIS, carrier control, sham stimulation). tTIS was delivered for 20 minutes using two high-frequency signals at 1000 Hz and 1000 Hz + IAF, whereas the carrier control used two 1000-Hz signals without an envelope modulation. EEG was recorded before and after stimulation during a visual vigilance task. Individual electric-field distributions in the occipital cortex were estimated using structural MRI-based finite-element simulations. A significant main effect of stimulation condition on the change in occipital alpha power was observed (F(2,32) = 5.69, p = .008, eta2p = .26). Post-hoc comparisons showed a significantly greater increase in alpha power following tTIS compared with both the carrier control (mean difference = 0.30, adjusted p = .036, Cohens d = 0.686) and sham stimulation (mean difference = 0.31, adjusted p = .037, Cohens d = 0.683). Carrier and sham conditions did not differ (adjusted p = 1.000). No behavioral effects were observed. The magnitude of the alpha-power change was not significantly associated with simulated electric-field strength in the occipital target region. tTIS was well tolerated, with no stimulation-related study discontinuations. tTIS targeting the occipital cortex therefore produced significant post-stimulation enhancement of alpha power beyond both sham and high-frequency carrier stimulation. The absence of an effect in the carrier condition supports the interpretation that the electrophysiological aftereffect depends on temporal interference rather than high-frequency stimulation components alone. These findings provide evidence for frequency-specific modulation of cortical oscillations by tTIS and support further investigation of its underlying mechanisms and stimulation parameters.

neuroscience↗

bioRxiv2026

Does Pre-Sensorimotor Brain Activity Modulate TMS-Evoked Potentials?

Transcranial magnetic stimulation combined with electroencephalography (TMS-EEG) provides a direct measure of cortical responses to local brain perturbations and offers a powerful approach for investigating brain-state-dependent neural dynamics. However, it remains unclear to what extent ongoing sensorimotor brain activity influences TMS-evoked potentials (TEPs). To address this question, thirty healthy participants performed kinesthetic motor imagery of left- and right-index finger tapping while single-pulse TMS was applied over the left primary motor cortex. 64-channel EEG was recorded to characterize sensorimotor oscillatory activity and TEPs. Time-frequency analyses quantified event-related desynchronization (ERD) in the mu (8-12 Hz) and beta (13-30 Hz) frequency bands, while TEP amplitudes were examined within early latency windows (10-65 ms). Motor imagery induced robust bilateral mu- and beta-band ERD, confirming successful engagement of the sensorimotor network. However, ERD patterns were highly similar between left- and right-hand motor imagery, and neither frequentist nor bayesian analyses identified differences in TMS-evoked potentials between imagery conditions. Source reconstruction demonstrated rapid propagation of TMS-evoked activity from the stimulated motor cortex to distributed bilateral motor regions. Correlation analyses revealed that greater pre-stimulus beta-band ERD was associated with larger P60 amplitudes. Because the instructed motor imagery conditions did not produce distinguishable pre-stimulus brain states, an exploratory trial-by-trial analysis was subsequently performed to account for naturally occurring variability in sensorimotor lateralization to investigate the effect of variability in ERD on TRP. This analysis revealed an overall effect of trial-by-trial brain state on TEP amplitudes

neuroscience↗

bioRxiv2026

Efficient capture-recapture inference for spatially varying natal dispersal,survival and recruitment

1. Natal dispersal is a key process in population ecology because it links local demographic processes to broader-scale population dynamics by redistributing individuals. When using capture-recapture data, multistate capture-recapture models using discrete spatial units as states are the gold standard for estimating natal dispersal among spatial units while accounting for spatial variation in survival, recruitment and imperfect detection. However, because their computational cost increases rapidly with the number of spatial units, applications have been limited to a small number of units. Therefore, in practice, these models cannot provide spatially detailed inference on natal dispersal across large landscapes. 2. We develop a computationally efficient Bayesian capture-recapture model, called the efficient natal dispersal (END) model, to estimate natal dispersal among discrete spatial units jointly with spatial variation in demographic parameters and detection probabilities. The END model relies on two key structural features: juveniles and breeders are separated into two arrays, and resightings outside the natal spatial unit are aggregated over time for individuals released as juveniles. 3. Using simulations, we show that the END model is considerably (up to 30 times) more computationally efficient than a conventional multistate model, while maintaining comparable parameter accuracy. We then apply the END model to white stork (Ciconia ciconia) capture-recapture data from Germany across 101 hexagonal spatial units, a spatial resolution at which a conventional multistate model is computationally infeasible. We estimate natal dispersal among units jointly with spatial variation in survival and recruitment. This allows us to identify areas of lower or higher survival, earlier or delayed recruitment, and dispersal probabilities among all units. By combining estimated dispersal probabilities with existing data on the number of juveniles born in each spatial unit, we estimate natal dispersal in terms of numbers of individuals and identify units with positive or negative net migration, sources and sinks. 4. Overall, our approach moves capture-recapture analyses from estimating natal dispersal among a few spatial units to inferring dispersal networks and assessing their demographic consequences across large domains. Our approach is applicable to many spatially structured capture-recapture datasets, opening new opportunities for studying spatial population dynamics.

ecology↗

bioRxiv2026

Time-resolved inference of gene regulatory networks underlying human cranial neural crest development suggests novel risk genes for orofacial clefting.

Cranial neural crest cells (CNCCs) play a central role in shaping the human head and face. Aberrant CNCC differentiation contributes to craniofacial birth defects, particularly non-syndromic cleft lip with or without cleft palate (nsCL/P), one of the most common congenital disorders. Although the number of genetic variants associated with this condition is steadily increasing, it remains challenging to determine if and how these variants may contribute to disease development. The majority of these variants lie within non-coding regulatory elements that govern cell-type and stage-specific gene expression, which is orchestrated by dynamic gene regulatory networks (GRNs). Despite extensive work in model organisms, a time-resolved, multi-omics perspective of GRNs controlling CNCC differentiation in a human system is still lacking. To fill this gap, we generated paired transcriptomic and chromatin accessibility data at four timepoints during in vitro differentiation of CNCCs derived from human induced pluripotent stem cells. Integrating these two modalities enabled time-resolved inference of GRNs and identification of dynamic regulatory relationships, including stage-specific roles of core transcription factors. Leveraging these time-resolved GRNs, we mapped 29 nsCL/P associated variants linked to 70 putative target genes, with 40 located outside the associated genomic loci, suggesting novel distal regulatory relationships. Integration of these data with complementary time-course scRNA-seq data revealed an ectomesenchymal-biased subpopulation of CNCCs as particularly sensitive to genetic variants associated with nsCL/P. We provide a time-resolved inference of GRN in human CNCC differentiation, allowing us to determine the dynamics of stage-specific core regulatory programs that are otherwise missed in analyses based on a single time snapshot. To our knowledge, the data represent the first multi-omics map of human CNCC with temporal resolution, which expands the understanding of early human craniofacial development, refines variant-to-gene assignment, prioritizes candidate risk genes and cell states relevant to nsCL/P. Our findings demonstrate the relevance of studying the dynamics upon differentiation rather than just one fixed timepoint and offer a valuable basis for further investigation of non-coding variation in CNCC-related disorders.

bioinformatics↗

bioRxiv2026

Identifying Treatment Related Signatures In Glioblastoma Using KaleidoCell

Understanding how transcriptional heterogeneity is organized across tumors, patients, and treatment conditions remains a central challenge in cancer biology. Here, we present kaleidoCell, a GPU-accelerated Python framework for consensus non-negative matrix factorization that identifies reproducible meta-programs across independent samples. When benchmarked against its principal counterpart, the geneNMF R package, kaleidoCell achieves a twofold speed improvement on large datasets. In addition, it includes an integrated analysis module that generates a comprehensive HTML report containing key results and visualizations--including marker genes corresponding to the meta-programs, gene set enrichment analysis, UMAP projections and violin plots--without requiring additional user code. Using glioblastoma as a case study, we applied kaleidoCell to two published datasets. In a panobinostat-treated cohort, kaleidoCell resolves the cellular landscape of the tumor microenvironment and delineates how HDAC inhibition reshapes malignant cell states at single-cell resolution. We extend prior descriptions of the metallothionein-associated stress program in treatment response and identify co induction of IER3 as a candidate component of the associated survival signalling. In addition, we uncover novel transcriptional signatures associated with HDAC inhibition. Beyond confirming suppression of a neural progenitor cell-/oligodendrocyte progenitor cell-like program which is consistent with prior reports, kaleidoCell identifies loss of an astrocyte-like identity program as a previously unrecognized candidate mechanism of panobinostat action in glioblastoma. Together, these results establish kaleidoCell as a fast, user-friendly framework that enables robust discovery of biologically meaningful transcriptional programs in large, heterogeneous single-cell datasets.

bioinformatics↗

bioRxiv2025

High pathogenicity avian influenza virus H5N1 (clade 2.3.4.4b) drives mass mortality in Eurasian crane (Grus grus) populations in Germany, 2025

In autumn 2025, an unprecedented mass mortality event was observed among the western migrating subpopulation of Eurasian cranes (Grus grus) in Germany. Systemic infection with highly pathogenic avian influenza virus H5N1, clade 2.3.4.4b, genotype DI.2.1, was identified as the cause of acute death. The gregarious behaviour of cranes at feeding and resting sites likely has contributed to the rapid and massive dissemination of viruses within the crane population.

ecology↗

bioRxiv2025

In-ear-tACS: Auditory Perception and Side Effects depend on Electrode Montage, Frequency, and DC-Offset

BackgroundNon-invasive transcranial alternating current stimulation (tACS) of the cochlea might be a promising new therapeutic option for patients with chronic tinnitus. However, electric stimulation of small, sensitive target regions, such as the inner ear, can cause adverse side effects (SEs). ObjectiveTo identify stimulation parameters with low side-effect profiles while reliably stimulating the cochlea, thereby improving patient comfort and safety and paving the way for the development of a medical device for treating patients with chronic tinnitus. ApproachHearing-healthy participants were stimulated with electrodes in the ear canal. Stimulation of the cochlea elicits a soft hearing impression (HI) in participants, indicating successful stimulation of the early auditory pathway. We systematically compare HS and SEs across distinct electrode configurations and stimulation parameters, including stimulation frequency and the presence of a Direct Current (DC)-offset. We record SE occurrence via visual analog scales after stimulation. Main ResultsWe find that tACS stimulation between 250 Hz and 2000 Hz reliably elicits HIs in participants. SEs are generally low. No occurrence of SEs resulted in participant withdrawal or severe adverse events, with only phosphenes, skin tingling, and a sense of vibration being reported as impactful. The addition of a slight DC-offset increases the occurrence and magnitude of SEs considerably. SignificanceOur results demonstrate the feasibility of tACS in non-invasively stimulating the auditory pathway with minimal adverse SE. Stimulation parameters with a low SE profile can be applied in further studies with tinnitus patients.

neuroscience↗

bioRxiv2025

Outbreak dynamics of high pathogenicity avian influenza virus H5N1, clade 2.3.4.4b euBB, in black-headed gulls and common terns in Germany in 2023

Since winter 2022/23, high pathogenicity avian influenza virus (HPAIV) H5N1 clade 2.3.4.4b, genotype euBB, has caused extensive mortality among wild birds. This genotype emerged in France in spring 2022 through reassortment between a gull-adapted low-pathogenicity virus and HPAIV H5N1. Phylogeographic and spatiotemporal analyses show that transmission into German breeding colonies of black-headed gulls (Chroicocephalus ridibundus) and common terns (Sterna hirundo) involved multiple independent incursions, likely via black-headed gulls returning from wintering grounds in the Netherlands, Belgium, and France. It spilled over into common terns, which breed in shared colonies with black-headed gulls, and led to high adult mortality in both species in 2023 (at least 8,137 black-headed gulls and 614 common terns; >3% of the breeding population), followed by significant breeding pair declines in 2024 (-15.9% in black-headed gulls, -5.8% in common terns). Increased immunity, at least in common terns, may have contributed to the apparent fade-out of genotype euBB. These findings highlight how integrating ornithological, epidemiological, and virological data can aid our understanding of viral transmission routes and population-level impacts, while also stressing that HPAIV should be added to the growing list of pressures on seabirds, a group that was already the most threatened among all bird taxa globally. Research Highlights- HPAIV H5N1 euBB caused mass mortality in gulls and terns in Germany in 2023 - Multiple independent viral incursions occurred into different parts of Germany - Serology showed survival and rising H5-seroprevalence in common terns - Outbreaks reduced the black-headed gull breeding populations by up to 24%

ecology↗

bioRxiv2025

Tracking biological hallucinations in single-cell perturbation predictions using scArchon, a comprehensive benchmarking platform

The accurate prediction of cellular responses to perturbations, such as drug treatments, remains a pivotal challenge in single-cell transcriptomics. While numerous deep learning tools have been developed for this task, their systematic benchmarking across diverse datasets and performance metrics has been limited. Here, we present scArchon, a reproducible, modular benchmarking platform built on Snakemake, designed to evaluate perturbation response prediction tools in an unbiased and extensible manner. Employing four representative single-cell RNA-seq datasets, we compare leading methods such as scGen, CPA, trVAE, scPRAM, scVIDR, scDisInFact, SCREEN, scPreGAN, and CellOT against baselines. We assess model performance using a composite of statistical and biological metrics. Our analysis reveals heterogeneous performance: while methods like trVAE, scGen, scPRAM, and scVIDR achieve robust results across multiple datasets, other tools occasionally underperform even compared to linear or control baselines. Notably, models with favorable quantitative scores may fail to retain key biological perturbation signatures, underscoring the need for gene-level evaluation. scArchon provides a unified, extensible foundation for large-scale, standardized benchmarking of perturbation prediction tools, facilitating methodological transparency and accelerating development in this rapidly evolving field. We encourage adoption of scArchon and sharing of containerized tools to drive progress in single-cell perturbation modeling.

bioinformatics↗

bioRxiv2025

The hepatitis E virus capsid protein ORF2 counteracts cell-intrinsic antiviral responses to enable persistence in hepatocytes

Hepatitis E virus (HEV) is a significant human pathogen causing both acute and chronic infections worldwide. The cell-intrinsic antiviral response serves as the initial defense against viruses and has been shown to be activated upon HEV infection. HEV can replicate in the presence of this response, but the underlying mechanisms remain poorly understood. Here, we investigated the role of the HEV structural proteins ORF2 and ORF3 in immunocompetent cells. Mechanistically, we validated that ectopic ORF2, but not ORF3, interfered with antiviral and inflammatory signaling downstream of pattern recognition receptors, in part through interaction with the central adaptor protein TANK binding kinase 1. In the full-length viral context, ORF2 contributed to a reduced antiviral response and consequently, more efficient viral replication. In addition, we discovered a protective mechanism mediated by ORF2 that shielded viral replication from antiviral effectors. Using single-cell RNA-sequencing, we confirmed that the presence of ORF2 in infected cells dampened antiviral responses in both actively infected cells and bystanders. As a consequence, we found that early in the infection process, the progression of authentic HEV infection relied on the presence of ORF2, facilitating a balance between viral replication and the antiviral response within immunocompetent cells. Altogether, our findings shed new light on the multifaceted role of ORF2 in the HEV life cycle and improve our understanding of the determinants that may contribute to HEV persistence. Significance statementHepatitis E virus (HEV) is an important yet often underestimated pathogen. Depending on the genotype, HEV infections can progress to chronicity, but the underlying mechanisms remain poorly understood. To gain insight into potential determinants, we investigated how HEV evades the bodys first line of defense, the cell-intrinsic antiviral response. We discovered that the HEV capsid protein ORF2 is crucial in limiting this response by interfering with antiviral signaling pathways and shielding viral replication from immune effectors. This balance between viral replication and the antiviral response contributes to persistent HEV infection in immunocompetent cells. Our findings reveal a new role for the HEV capsid protein in the viral life cycle and highlight it as an important target for novel therapeutic approaches.

microbiology↗

bioRxiv2024

Concomitant suppression of COX-1 and COX-2 is insufficient to induce enteropathy associated with chronic NSAID use

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most widely used medications for the management of chronic pain; however, they are associated with numerous gastrointestinal (GI) adverse events. Although many mechanisms have been suggested, NSAID-induced enteropathy has been thought to be primarily due to inhibition of both cyclooxygenases (COX) -1 and -2, which results in suppression of prostaglandin synthesis. Yet surprisingly, we found that concomitant postnatal deletion of Cox-1 and -2 over 10 months failed to cause intestinal injury in mice unless they were treated with naproxen or its structural analog, phenylpropionic acid, which is not a COX inhibitor. Cox double knockout mice exhibit a distinct gut microbiome composition and cohousing them with controls rescues their dysbiosis and delays the onset of NSAID-induced GI bleeding. In both the UK Biobank and All of Us human cohorts, coadministration of antibiotics with NSAIDs is associated with an increased frequency of GI bleeding. These results show that prostaglandin suppression plays a trivial role in NSAID-induced enteropathy. However, Cox deletion causes dysbiosis of the gut microbiome that amplifies the enteropathic response to NSAIDs.

pharmacology and toxicology↗

bioRxiv2024

Prediction of context-specific regulatory programs and pathways using interpretable deep learning

Variational autoencoders (VAEs) are being widely adopted for the analysis of single-cell RNA sequencing (scRNA-seq) data. As with any non-linear models, however, they lack interpretability, which is a crucial aspect in the biomedical field where researchers want to be able to trust their model predictions. Our previously developed OntoVAE model addressed this issue by integrating biological ontologies in the decoder, which made the neuronal activations correspond to pathway activities. However, when multiple covariates are present, disentangling their relative contributions is challenging. To address this limitation, we developed COBRA, a VAE tool that combines the interpretable decoder part of OntoVAE with an adversarial approach that separates covariate effects in the latent space. In this work, we demonstrate the use of COBRA on two different scRNA-seq datasets in different contexts. We applied the tool to an interferon stimulated mouse dataset to separate the effects of celltype and treatment on transcription factors and biological pathways. We furthermore showed how COBRA can be used to predict the state of unseen celltypes.

bioinformatics↗

bioRxiv2024

Stress from environmental change drives clearance of a persistent enteric virus

Persistent viral infections are associated with long-term health issues and prolonged transmission. How external perturbations after initial exposure affect the duration of infection is unclear. We discovered that murine astrovirus, an enteric RNA virus, persists indefinitely when mice remain unperturbed but is cleared rapidly after cage change. Besides eliminating the external viral reservoir, cage change also induced a transcriptional defense response in the intestinal epithelium. We further identified that displacing infected animals initially caused a temporary period of immune suppression through the stress hormone corticosterone, which was followed by an immune rebound characterized by an increase in CD8 T cells responsible for the epithelial antiviral responses. Our findings show how viral persistence can be disrupted by preventing re-exposure and activating immunity upon stress recovery, indicating that external factors can be manipulated to shorten the duration of a viral infection.

microbiology↗

bioRxiv2023

Pathogen-prey-predator relations of avian raptors during epizootics of highly pathogenic avian influenza virus HPAIV H5N1 (clade 2.3.4.4b) in Germany

Transition of highly pathogenic clade 2.3.4.4b H5 avian influenza virus (HPAIV) from epizootic to enzootic status in Northern European countries was associated with severe losses and even mass mortalities among various wild bird species. Both avian and mammalian raptors hunting infected debilitated birds or scavenging on virus-contaminated avian carcasses contracted HPAIV infection. This precarious pathogen-prey-predator relation further worsened when in 2021 and 2022 outbreaks in Germany overlapped with the hatching season of avian raptor species. Retro- and prospective surveillance revealed avian raptors as important indicators of HPAIV and its genetic diversity on the one hand. On the other hand, their role as victims of HPAIV is stipulated. The first case of an HPAIV H5N1-related death of a white-tailed sea eagle (Haliaeetus albicilla; WTSE) hatch in Germany, 2021, followed by several such cases in 2022, and a low overall seropositivity rate of 5.0-7.9% among WTSE nestlings, raised fears of a serious negative impact on reproduction rates of WTSEs and other birds of prey when HPAIV becomes enzootic in an ecosystem. However, comparably stable breeding success of WTSE in the study area in 2022 and a potentially evolving natural immunity raises hope for a less severe long-term impact. Article impact statementAdapted surveillance measures were developed to assess risks for the conservation of avian raptors due to the panzootic spread of HPAIV.

microbiology↗

bioRxiv2023

A network of transcriptomic signatures identifies novel comorbidity mechanisms between schizophrenia and somatic disorders

The clinical burden of mental illness, in particular schizophrenia and bipolar disorder, are driven by frequent chronic courses and increased mortality, as well as the risk for comorbid conditions such as cardiovascular disease and type 2 diabetes. Evidence suggests an overlap of molecular pathways between psychotic disorders and somatic comorbidities. In this study, we developed a computational framework to perform comorbidity modeling via an improved integrative unsupervised machine learning approach based on multi-rank non-negative matrix factorization (mrNMF). Using this procedure, we extracted molecular signatures potentially explaining shared comorbidity mechanisms. For this, 27 case-control microarray transcriptomic datasets across multiple tissues were collected, covering three main categories of conditions including psychotic disorders, cardiovascular diseases and type II diabetes. We addressed the limitation of normal NMF for parameter selection by introducing multi-rank ensembled NMF to identify signatures under various hierarchical levels simultaneously. Analysis of comorbidity signature pairs was performed to identify several potential mechanisms including 1) dysfunction of endothelial systems; 2) induction of hypoxia and oxidative stress; 3) dysregulation of neural transmission GABAergic system associated with neuroendocrine function (e.g. insulin secretion); 4) activation of inflammatory response auxiliarily interconnecting blood-brain systems, oxidative response and GABAergic neuro-action. Overall, we proposed a general cross-cohorts computing workflow for investigating the comorbid pattern across multiple symptoms, applied it to the real-data comorbidity study on schizophrenia, and further discussed the potential for future application of the approach.

bioinformatics↗

bioRxiv2023

Elucidating the activation mechanism for GBP1 oligomerization

The dynamin-related human guanylate-binding protein 1 (GBP1) mediates host defense against microbial pathogens. Upon GTP binding and hydrolysis, auto-inhibited GBP1 monomers dimerize and assemble into soluble and membrane-bound oligomers, which are crucial for innate immune responses. How higher-order GBP1 oligomers are built from dimers and how assembly is coordinated with nucleotide-dependent conformational changes has remained elusive. Here, we present cryo-electron microscopy-based structural data of the soluble and membrane-bound GBP1 oligomers demonstrating that GBP1 assembles in an outstretched dimeric conformation. We identify a surface-exposed helix in the large GTPase domain, which contributes to the oligomerization interface, and probe its nucleotide- and dimerization-dependent movements facilitating the formation of an antimicrobial protein coat on a Gram-negative bacterial pathogen. Our results reveal a sophisticated activation mechanism for GBP1 in which nucleotide-dependent structural changes coordinate dimerization, oligomerization, and membrane binding to allow encapsulation of pathogens with an antimicrobial protein coat.

biochemistry↗

bioRxiv2023

Highly pathogenic avian influenza causes mass mortality in Sandwich tern (Thalasseus sandvicensis) breeding colonies across northwestern Europe

AO_SCPLOWBSTRACTC_SCPLOWIn 2022, highly pathogenic avian influenza (HPAI) A(H5N1) virus clade 2.3.4.4b became enzootic and caused mass mortality in Sandwich terns and other seabird species across northwestern Europe. We present data on characteristics of the spread of the virus between breeding colonies and the number of dead adult Sandwich terns recorded at breeding sites throughout northwestern Europe. Within two months after the first mortalities were reported, in total 20,531 adult Sandwich terns were found dead, which is >17% of the total northwestern European breeding population. Losses are likely higher, as we expect that many victims were not found (mortality rate might be up to 74% of the breeding population). Inside the colonies almost all chicks died. After the peak of the outbreak, in a colony established by late breeders, 25.7% of adults showed immunity against HPAI subtype H5. Removal of carcasses helped in reducing the spread of the disease and consequently total mortality. More research on the sources and modes of transmission, incubation times, effective containment and immunity is urgently needed to combat this major threat for colonial seabirds.

ecology↗

bioRxiv2023

Genetic and Environmental interactions contribute to immune variation in rewilded mice

The relative and synergistic contributions of genetics and environment to inter-individual immune response variation remain unclear, despite its implications for understanding both evolutionary biology and medicine. Here, we quantify interactive effects of genotype and environment on immune traits by investigating three inbred mouse strains rewilded in an outdoor enclosure and infected with the parasite, Trichuris muris. Whereas cytokine response heterogeneity was primarily driven by genotype, cellular composition heterogeneity was shaped by interactions between genotype and environment. Notably, genetic differences under laboratory conditions can be decreased following rewilding, and variation in T cell markers are more driven by genetics, whereas B cell markers are driven more by environment. Importantly, variation in worm burden is associated with measures of immune variation, as well as genetics and environment. These results indicate that nonheritable influences interact with genetic factors to shape immune variation, with synergistic impacts on the deployment and evolution of defense mechanisms.

immunology↗