Diseases Research Articles

Neurotropic Tick-Borne Flavivirus in Alpine Chamois (Rupicapra rupicapra rupicapra), Austria, 2017, Italy, 2023

The European subtype of tick-borne encephalitis virus (TBEV-Eur; species Orthoflavivirus encephalitidis, family Flaviviridae) was the only tick-borne flavivirus present in central Europe known to cause neurologic disease in humans and several animal species. Here, we report a tick-borne flavivirus isolated from Alpine chamois (Rupicapra rupicapra rupicapra) with encephalitis and attached ticks, present over a wide area in the Alps. Cases were detected in 2017 in Salzburg, Austria, and 2023 in Lombardy and Piedmont, Italy. The virus strains exhibit 94.8–97.3% nucleotide identities to each other and are more closely related to Louping ill viruses (LIV; Orthoflavivirus loupingi; 90–92% identities) than to TBEV-Eur (less than 88%). The chamois-derived virus strains, tentatively termed “Alpine chamois encephalitis virus”, form a well-supported independent genetic clade with Spanish goat encephalitis virus, clearly separated from other LIV. This supports its designation as a new virus subtype with the proposed shared taxonomic name “Spanish goat and Alpine chamois encephalitis virus subtype” within the species Orthoflavivirus loupingi. The zoonotic potential of this newly identified virus subtype as well as its host range in other animal species including farm animals needs to be further investigated.

What a tangled web we weave: crosstalk between JAK–STAT and other signalling pathways during development in Drosophila

The Janus kinase–signal transducer and activator of transcription (JAK–STAT) signalling pathway is a key player in animal development and physiology. Although it functions in a variety of processes, the net output of JAK–STAT signalling depends on its spatiotemporal activation, as well as extensive crosstalk with other signalling pathways. Drosophila, with its relatively simple signal transduction pathways and plethora of genetic analysis tools, is an ideal system for dissecting JAK–STAT signalling interactions. In this review, we explore studies in Drosophila revealing that JAK–STAT signalling lies at the nexus of a complex network of interlinked pathways, including epidermal growth factor receptor (EGFR), c‐Jun N‐terminal kinase (JNK), Notch, Insulin, Hippo, bone morphogenetic protein (BMP), Hedgehog (Hh) and Wingless (Wg). These pathways can synergise with or antagonise one another to produce a variety of outcomes. Given the conserved nature of signal transduction pathways, we conclude with our perspective on the implication of JAK–STAT signalling dysregulation in human diseases, and how studies in Drosophila have the potential to inform and influence clinical research.

Fabrication of MoS2@Fe3O4 Magnetic Catalysts with Photo-Fenton Reaction for Enhancing Tetracycline Degradation

Tetracycline (TCs) is widely used in the treatment of human and animal infectious disease. TCs gives rise to a growing threat to the human health and environment protection due to its overuse. Therefore, it is important to remove TCs contaminants from waste effluents. In this work, MoS2@Fe3O4 catalytic material was fabricated by the simple hydrothermal method, which was applied in the photo-Fenton system to degrade TCs. The crystal structure, surface morphology, elemental composition, chemical state, electrochemical properties, and separability of MoS2@Fe3O4 catalytic materials were analyzed by X-ray diffraction (XRD), scanning electron microscope (SEM), conventional and high-resolution transmission electron microscopy (TEM/HRTEM), X-ray photoelectron spectroscopy (XPS), electrochemical impedance spectroscopy (EIS), and vibrating sample magnetometry (VSM). Furthermore, MoS2@Fe3O4 could degrade 98.6% of TCs within 60 min under the optimum reaction conditions (the catalyst dosage of 3 g/L, H2O2 concentration of 5 mmol/L, the initial TCs concentration of 50 mg/L, and the initial pH of 5), which was a significant increase compared with pure Fe3O4. MoS2 can accelerate the Fe3+/Fe2+ cycle through electron transfer from Mo4+ to Fe3+, resulting in the improvement in the degradation efficiency of TCs. The quenching and electron paramagnetic resonance (EPR) results showed that OH• and photogenic hole h+ was the main active species in the photo-Fenton system. What is more, MoS2@Fe3O4 catalytic materials had remarkable stability and reusability, and can be handily regained via magnetic separation technology in a real scenario.

Mechanisms of Copper-Induced Autophagy and Links with Human Diseases

As a structural and catalytic cofactor, copper is involved in many biological pathways and is required for the biochemistry of all living organisms. However, excess intracellular copper can induce cell death due to its potential to catalyze the generation of reactive oxygen species, thus copper homeostasis is strictly regulated. And the deficiency or accumulation of intracellular copper is connected with various pathological conditions. Since the success of platinum-based compounds in the clinical treatment of various types of neoplasias, metal-based drugs have shown encouraging perspectives for drug development. Compared to platinum, copper is an essential intracellular trace element that may have better prospects for drug development than platinum. Recently, the potential therapeutic role of copper-induced autophagy in chronic diseases such as Parkinson’s, Wilson’s, and cardiovascular disease has already been demonstrated. In brief, copper ions, numerous copper complexes, and copper-based nano-preparations could induce autophagy, a lysosome-dependent process that plays an important role in various human diseases. In this review, we not only focus on the current advances in elucidating the mechanisms of copper or copper-based compounds/preparations on the regulation of autophagy but also outline the association between copper-induced autophagy and human diseases.

Correlation Between Cryptococcus Infection and the Nasal Mycobiota in a Population of Free-Ranging Koalas (Phascolarctos cinereus) in New South Wales, Australia

Cryptococcosis is a fungal disease in humans and animals, caused by the Cryptococcus neoformans and Cryptococcus gattii species complexes. Clinical cryptococcosis primarily manifests as upper respiratory tract disease; however, dissemination to other organs, particularly the brain, can occur. Nasal colonisation and subclinical cryptococcosis are common in koalas (Phascolarctos cinereus) due to their shared environmental niche with Cryptococcus: Eucalyptus trees. However, for reasons that remain unclear, the prevalence of clinical disease is low in koalas. Interactions between respiratory pathogens and the nasal mycobiome are thought to play a role in the development and progression of numerous respiratory diseases. As such, this study aimed to characterise the mycobiome of the nasal vestibule in koalas with and without evidence of cryptococcal colonisation and subclinical disease via the next-generation sequencing (NGS) of the ITS1 region of the fungal internal transcribed spacer (ITS) gene. Samples were collected from 47 koalas from a population of free-ranging koalas in the Liverpool Plains, NSW, Australia, with a known history of Cryptococcus exposure and nasal colonisation. Of the 47 animals tested, 6.4% were culture-positive only, 4.3% were seropositive only, and 2.1% were culture- and seropositive. C. gattii was detected in four samples via NGS. C. neoformans was not detected via NGS. There were no significant differences in the nasal mycobiomes of Cryptococcus-positive and -negative animals; thus, we could not establish a definitive association between the mycobiome and infection outcomes. We identified a number of fungal genera that were significantly more abundant in samples from Cryptococcus-positive animals, but there was no apparent relationship between these genera and the development of cryptococcosis. This study represents the first investigation of the nasal mycobiota of wild koalas. Further studies involving koalas with clinical disease are necessary to determine the role of the nasal mycobiota in the development of cryptococcosis.

Decoding Extracellular Protein Glycosylation in Human Health and Disease

Protein glycosylation, the covalent attachment of carbohydrate, or glycan, structures onto the protein backbone, is one of the most complex and heterogeneous post-translational modifications (PTMs). Extracellular protein glycosylation, in particular N- and mucin-type O-glycosylation, plays pivotal roles in a number of biophysical and biochemical processes, such as protein folding and stability, cell adhesion, signaling, and protection. As such, aberrant glycosylation is implicated in a variety of diseases, including cancer. However, the nontemplated nature and structural heterogeneity of protein glycosylation hinder glycoprotein characterization with traditional methods. Recent advances in analytical techniques have improved capabilities for decoding glycan complexity, a promising step toward understanding the role of glycosylation in human health and disease. In this review, we highlight key and emerging techniques to study protein glycosylation, and we emphasize how these techniques have improved our understanding of glycosylation in a biologically relevant context.

Causality-driven candidate identification for reliable DNA methylation biomarker discovery

Despite vast data support in DNA methylation (DNAm) biomarker discovery to facilitate health-care research, this field faces huge resource barriers due to preliminary unreliable candidates and the consequent compensations using expensive experiments. The underlying challenges lie in the confounding factors, especially measurement noise and individual characteristics. To achieve reliable identification of a candidate pool for DNAm biomarker discovery, we propose a Causality-driven Deep Regularization framework to reinforce correlations that are suggestive of causality with disease. It integrates causal thinking, deep learning, and biological priors to handle non-causal confounding factors, through a contrastive scheme and a spatial-relation regularization that reduces interferences from individual characteristics and noises, respectively. The comprehensive reliability of the proposed method was verified by simulations and applications involving various human diseases, sample origins, and sequencing technologies, highlighting its universal biomedical significance. Overall, this study offers a causal-deep-learning-based perspective with a compatible tool to identify reliable DNAm biomarker candidates, promoting resource-efficient biomarker discovery.

Enantioselective OTUD7B fragment discovery through chemoproteomics screening and high-throughput optimisation

Deubiquitinating enzymes (DUBs) are key regulators of cellular homoeostasis, and their dysregulation is associated with several human diseases. The ovarian tumour protease (OTU) family of DUBs are biochemically well-characterised and of therapeutic interest, yet only a few tool compounds exist to study their cellular function and therapeutic potential. Here we present a chemoproteomics fragment screening platform for identifying novel DUB-specific hit matter, that combines activity-based protein profiling with high-throughput chemistry direct-to-biology optimisation to enable rapid elaboration of initial fragment hits against OTU DUBs. Applying these approaches, we identify an enantioselective covalent fragment for OTUD7B, and validate it using chemoproteomics and biochemical DUB activity assays.

The TRP Channels Serving as Chemical-to-Electrical Signal Converter

Biology uses many signaling mechanisms. Among them, calcium and membrane potential are two prominent mediators for cellular signaling. TRPM4 and TRPM5, two calcium-activated monovalent cation-conducting ion channels, offer a direct linkage between these two signals. Their activities convert a rise in the intracellular calcium level—a chemical signal—into depolarization of membrane potential—an electrical signal. Interestingly, membrane depolarization can in turn alter the electrical driving force or membrane permeability for calcium entry, hence offers feedback mechanisms for regulating calcium signaling. By converging two powerful cellular signals, TRPM4 and TRPM5 are capable of contributing to many fundamental biological processes including cardiovascular biology, immunology, insulin release, chemo-sensation, and others. Numerous mutations in TRPM4 are linked to human hereditary cardiac and skin diseases, whereas knocking out TRPM5 in mice abolishes perception of sweet, umami and bitter tastes. This review summarizes what are currently known about the signaling roles of these unique TRP channels, and what remain mysterious.

Complementary cognitive roles for D2-MSNs and D1-MSNs during interval timing.

The role of striatal pathways in cognitive processing is unclear. We studied dorsomedial striatal cognitive processing during interval timing, an elementary cognitive task that requires mice to estimate intervals of several seconds and involves working memory for temporal rules as well as attention to the passage of time. We harnessed optogenetic tagging to record from striatal D2-dopamine receptor-expressing medium spiny neurons (D2-MSNs) in the indirect pathway and from D1-dopamine receptor-expressing MSNs (D1-MSNs) in the direct pathway. We found that D2-MSNs and D1-MSNs exhibited distinct dynamics over temporal intervals as quantified by principal component analyses and trial-by-trial generalized linear models. MSN recordings helped construct and constrain a four-parameter drift-diffusion computational model in which MSN ensemble activity represented the accumulation of temporal evidence. This model predicted that disrupting either D2-MSNs or D1-MSNs would increase interval timing response times and alter MSN firing. In line with this prediction, we found that optogenetic inhibition or pharmacological disruption of either D2-MSNs or D1-MSNs increased interval timing response times. Pharmacologically disrupting D2-MSNs or D1-MSNs also changed MSN dynamics and degraded trial-by-trial temporal decoding. Together, our findings demonstrate that D2-MSNs and D1-MSNs had opposing dynamics yet played complementary cognitive roles, implying that striatal direct and indirect pathways work together to shape temporal control of action. These data provide novel insight into basal ganglia cognitive operations beyond movement and have implications for human striatal diseases and therapies targeting striatal pathways.

Integrated omics profiling of individual variations in intestinal damage to the soybean allergen in piglets

IntroductionA small number of soybean allergens [including Glycinin (11S) and β-Conglycinin (7S)] in the commercially available corn-soybean meal diet can still cause allergy in some weaned piglets, which may be the result of the interaction of genetic, and nutrition, but the specific mechanism is still unclear.MethodsIn this study, 20 allergic piglets and 20 non-allergic piglets were selected from 92 weaned piglets by skin sensitization tests, which were used to examine the whole sequence genome. The indicators related to humoral and cellular immunity, transcriptomics, and metabolomics analysis were determined by randomly selecting 5 boars in the allergic group and non-allergic group and then performing a validation in vitro.ResultsThe sensitization rate of soybean antigen in the corn-soybean meal diet was 21.74% and there was a gender difference with the sensitization rate of female pigs (31.34%) being higher than that of male pigs (13.23%). Moreover, the levels of inflammatory factors (IL-1β, IL-4, TNF-α) and antibodies (IgG, IgE, and specific IgG) in allergic piglets were significantly higher than those in non-allergic piglets (P < 0.05). Whole genome re-sequencing analysis revealed specific mutations in the exons and URT5 of TRAPPC2, PIR, CFP, and SOWAHD genes and showed significantly higher expression levels of related genes in the spleen of allergic piglets (P < 0.05). Transcriptome analysis identified IL17REL, CCL19, CD1E, CD1.1, etc. immune differential genes, metabolomics results showed that soybean antigen affected the utilization and metabolism of intestinal nutrients in piglets, mainly the digestion and absorption of protein and the synthesis and metabolism of amino acids. Transfection of CFP/TRAPPC2/CCL19 siRNA could partially alleviate the injury of RAW264.7 cells or IPEC-J2 cells induced by β-Conglycinin.ConclusionTherefore, the individual differences in intestinal damage induced by soybean antigen protein in the corn-soybean meal diet are closely related to PIR, CFP, TRAPPC2, SOWAHD, and CCL19 genes. Soybean antigens affect the intestinal nutrient utilization and metabolism of piglets, which provides a scientific reference for the study of soybean antigen sensitization mechanisms, precision nutrition, disease prevention, and control of piglets, and also lays a foundation for human foodborne diseases.

Use of Tick Cell Lines in Co-Infection Studies with a Preliminary Study of Co-Culture of Borrelia burgdorferi and Anaplasma phagocytophilum

Ixodes ricinus is an important vector of infectious human and livestock diseases in Europe. Co-infections of pathogens in ticks and hosts have been reported. Tick cell lines offer a useful model system for study of co-infections. We present a review of the existing literature on co-infections in tick cell lines. Previous studies have demonstrated the usefulness of tick cell lines in studies on co-infection of different pathogens and their interaction with the tick microbiome. We also carried out a preliminary study to investigate the effects of co-culturing Borrelia burgdorferi and Anaplasma phagocytophilum on their growth and interactions with the Ixodes ricinus cell line IRE/CTVM19 over a 13-day period. Replication of both pathogens was quantified by real-time PCR. The presence of A. phagocytophilum appeared to have a slight inhibitory effect on the multiplication of B. burgdorferi, that were added subsequently. In contrast, the prior presence of B. burgdorferi appeared to have a stimulatory effect on A. phagocytophilum after 6 days in culture. We conclude that the IRE/CTVM19 tick cell line is suitable for simultaneous and continuous cultivation of both bacteria and can be applied in future research.

Complementary cognitive roles for D2-MSNs and D1-MSNs during interval timing

The role of striatal pathways in cognitive processing is unclear. We studied dorsomedial striatal cognitive processing during interval timing, an elementary cognitive task that requires mice to estimate intervals of several seconds and involves working memory for temporal rules as well as attention to the passage of time. We harnessed optogenetic tagging to record from striatal D2-dopamine receptor-expressing medium spiny neurons (D2-MSNs) in the indirect pathway and from D1-dopamine receptor-expressing MSNs (D1-MSNs) in the direct pathway. We found that D2-MSNs and D1-MSNs exhibited distinct dynamics over temporal intervals as quantified by principal component analyses and trial-by-trial generalized linear models. MSN recordings helped construct and constrain a four-parameter drift-diffusion computational model in which MSN ensemble activity represented the accumulation of temporal evidence. This model predicted that disrupting either D2-MSNs or D1-MSNs would increase interval timing response times and alter MSN firing. In line with this prediction, we found that optogenetic inhibition or pharmacological disruption of either D2-MSNs or D1-MSNs increased interval timing response times. Pharmacologically disrupting D2-MSNs or D1-MSNs also changed MSN dynamics and degraded trial-by-trial temporal decoding. Together, our findings demonstrate that D2-MSNs and D1-MSNs had opposing dynamics yet played complementary cognitive roles, implying that striatal direct and indirect pathways work together to shape temporal control of action. These data provide novel insight into basal ganglia cognitive operations beyond movement and have implications for human striatal diseases and therapies targeting striatal pathways.

Characterizing SV40-hTERT Immortalized Human Lung Microvascular Endothelial Cells as Model System for Mechanical Stretch-Induced Lung Injury

Drug development for human disease relies on preclinical model systems such as human cell cultures and animal experiments before therapeutic treatments can ultimately be tested on humans in clinical studies. We here describe the generation of a novel human cell line (HLMVEC/SVTERT289) that we generated by transfection of microvascular endothelial cells from healthy donor lung tissue with the catalytic domain of telomerase and the SV40 large T/small t-antigen. These cells exhibited satisfactory growth characteristics and largely maintained their native characteristics, including morphology, cell surface marker expression, angiogenic potential and the protein composition of secreted extracellular vesicles. In order to test their suitability as a disease model, we simulated mechanical stress induced by cyclic stretch as encountered in ventilator-induced lung injury using the FlexCell® system and compared their performance to primary lung endothelial cells. In this setting, HLMVEC/SVTERT289 cells exhibited significantly higher neprilysin activity on the cell surface and extracellular vesicles secreted from the cell line exhibited higher Tissue Factor and ACE2 expression but lower ACE expression and ACE activity than vesicles released from the primary cells. This study provides an unprecedented and detailed characterization of the HLMVEC/SVTERT289 cell line, which should help to appraise its suitability in different molecular studies.

Antimicrobial Activities of Citrus Seed and Leaf Extracts Against Selected Bacterial and Fungal Pathogens Linked to Human Diseases: In vitro Experimental Study in Musanze, Rwanda

Antimicrobial resistance has caused major challenges in both bacterial and fungal infections. Therefore, the current study was designed to evaluate the antimicrobial activity with different crude extracts of leaves and seeds of Citrus limon against Gram-positive (Staphylococcus aureus), Gram-negative bacteria (Escherichia coli, Salmonella typhi, Pseudomonas aeruginosa) and fungi (Cryptococcus neoformans and Candida albicans) obtained from different clinical settings. Filtrate extracts after maceration technique and the phytochemical substances detected in plants were flavonoid, saponin, alkaloid, glycoside, and resin under investigation. In vitro, a disc diffusion assay was applied to measure the inhibition zone of the plant effect in millimeters (mm). It was observed that Citrus limon activity showed the highest on ethanolic seed against Staphylococcus aureus and the lowest activity plant observed on methanolic leaf extract against Klebsiella oxytoca. The mean values of Citrus limon extract convinced there was no statistically significant correlation among extract solvents used in the study (ρ > 0.05). Oxacillin was used as the positive control and discs without antibiotic content as the negative control during testing. To conclude, ethanolic seed extract has shown the highest effect against Staphylococcus aureus and Salmonella typhi from isolate. Indeed, plant extracts that showed potential effectiveness, such as (Citrus leaves and seeds) can be used as natural alternative preventive measures to control pathogenic bacterial diseases and prevent the rise of antibiotic resistance. Furthermore, studies to evaluate the in vivo potential in an animal model are recommended. Keywords: Citrus limon, Crude extract, Bacteria, Fungi, Antimicrobial resistance.

Approaches and applications in transdermal and transpulmonary gene drug delivery

Gene therapy has emerged as a pivotal component in the treatment of diverse genetic and acquired human diseases. However, effective gene delivery remains a formidable challenge to overcome. The presence of degrading enzymes, acidic pH conditions, and the gastrointestinal mucus layer pose significant barriers for genetic therapy, necessitating exploration of alternative therapeutic options. In recent years, transdermal and transpulmonary gene delivery modalities offer promising avenues with multiple advantages, such as non-invasion, avoided liver first-pass effect and improved patient compliance. Considering the rapid development of gene therapeutics via transdermal and transpulmonary administration, here we aim to summarize the nearest advances in transdermal and transpulmonary gene drug delivery. In this review, we firstly elaborate on current delivery carrier in gene therapy. We, further, describe approaches and applications for enhancing transdermal and transpulmonary gene delivery encompassing microneedles, chemical enhancers, physical methods for transdermal administration as well as nebulized formulations, dry powder formulations, and pressurized metered dose formulations for efficient transpulmonary delivery. Last but not least, the opportunities and outlooks of gene therapy through both administrated routes are highlighted.

Wpływ zmian klimatu na choroby skóry – narracyjny przegląd literatury

SUMMARY INTRODUCTION. Climate change has a significant impact on human health, particularly with regard to the respiratory, immune and cardiovascular systems. In addition, these changes have a significant impact on mental health and dermatological diseases. The main drivers of these health changes are increasing temperature, humidity, expansion of the ozone hole and increasing environmental pollution. Without corrective action, these trends will worsen. PURPOSE OF THE WORK. The purpose of this review is to present the current state of knowledge on the impact of climate change on the development of skin diseases in humans and to explore possible methods of their prevention. MATERIALS AND METHODS. A narrative review of the literature was conducted and an analysis of the literature retrieved from PubMed and Google Scholar databases was performed. Articles were searched using the keywords: "climate change", "environmental pollution", "UV radiation", "skin diseases". CONCLUSIONS. Climate change is associated with a significant increase in the incidence of various skin diseases, especially cancer, allergic diseases, infectious diseases and reactions after insect bites. The main cause of these changes is global warming, but increased pollution and the expansion of the "ozone hole" are also significant contributors to the increase in the number of diseases. Increased awareness of these trends enables faster diagnosis and treatment of lesions, as well as more effective prevention of new diseases.

Small CAG Repeat RNA Forms a Duplex Structure with Sticky Ends That Promote RNA Condensation.

Biomolecular condensation lays the foundation of forming biologically important membraneless organelles, but abnormal condensation processes are often associated with human diseases. Ribonucleic acid (RNA) plays a critical role in the formation of biomolecular condensates by mediating the phase transition through its interactions with proteins and other RNAs. However, the physicochemical principles governing RNA phase transitions, especially for short RNAs, remain inadequately understood. Here, we report that small CAG repeat (sCAG) RNAs composed of six to seven CAG repeats, which are pathogenic factors in Huntington's disease, undergo phase transition in vitro and in cells. Leveraging solution nuclear magnetic resonance spectroscopy and advanced coarse-grained molecular dynamic simulations, we reveal that sCAG RNAs form duplex structures with 3'-sticky ends, where the GC stickers initiate intermolecular crosslinking and promote the formation of RNA condensates. Furthermore, we demonstrate that sCAG RNAs can form cellular condensates within nuclear speckles. Our work suggests that the RNA phase transition can be promoted by specific structural motifs, reducing the reliance on sequence length and multivalence. This opens avenues for exploring new functions of RNA in biomolecular condensates and designing novel biomaterials based on RNA condensation.

Selected Mechanisms of Action of Bacteriophages in Bacterial Infections in Animals

Bacteriophages, as ubiquitous bacterial viruses in various natural ecosystems, play an important role in maintaining the homeostasis of the natural microbiota. For many years, bacteriophages were not believed to act on eukaryotic cells; however, recent studies have confirmed their ability to affect eukaryotic cells and interact with the host immune system. Due to their complex protein structure, phages can also directly or indirectly modulate immune processes, including innate immunity, by modulating phagocytosis and cytokine reactions, as well as acquired immunity, by producing antibodies and activating effector cells. They can therefore have a profound impact on the course of bacterial infections by stimulating and at the same time inhibiting the systemic pro-inflammatory response. This review article presents a characterization of the processes by which bacteriophages affect selected immune mechanisms in selected animal species. The results of our own experiments using calves are also presented as examples. The paper contains many new examples of potential uses of bacteriophages and their effects on eukaryotic cells, especially in the course of bacterial infections, which are extremely important in experimental treatments exploiting phages as alternatives to antibiotics. The positive results of the effects of bacteriophages on eukaryotic cells during infections open up promising new prospects for their use as natural tools in the treatment of bacterial, fungal, and viral diseases in animals and humans.

Animal Models for Human-Pathogenic Coronavirus and Animal Coronavirus Research

Coronavirus epidemics have posed a serious threat to both human and animal health. To combat emerging infectious diseases caused by coronaviruses, various animal infection models have been developed and applied in research, including non-human primate models, ferret models, hamster models, mouse models, and others. Moreover, new approaches have been utilized to develop animal models that are more susceptible to infection. These approaches include using viral delivery methods to induce the expression of viral receptors in mouse tissues and employing gene-editing techniques to create genetically modified mice. This has led to the successful establishment of infection models for multiple coronaviruses, significantly advancing related research. In contrast, livestock and pets that can be infected by animal coronaviruses provide valuable insights when used as infection models, enabling the collection of accurate clinical data through the analysis of post-infection pathological features. However, despite the potential insights, there is a paucity of research data pertaining to these infection models. In this review, we provide a detailed overview of recent progress in the development of animal models for coronaviruses that cause diseases in both humans and animals and suggest ways in which animal models can be adapted to further enhance their value in research.