is a Gram-negative bacterium isolated from the feces of bats, and there is a scarcity of information regarding its genomic and pathogenicity characteristics. This study systematically evaluated the pathogenic potential of . by comparing the survival rates, bacterial loads in the peripheral blood and organs, histopathological lesions, and the production of proinflammatory cytokines in C57BL/6 mice infected with strains HY037 and HY041 of . . The findings revealed that mice infected with . had low survival rates, with significant differences between the HY041 and HY037 strains. The mice infected with HY041 exhibited more severe pulmonary histopathological damage and higher levels of proinflammatory cytokines compared to those infected with HY037. These results demonstrated that . is lethal in mice, causing significant pulmonary histopathological damage accompanied by the dysregulated secretion of proinflammatory cytokines in lung tissues and blood. The molecular mechanisms underlying their virulence were investigated through comparative analyses of the genomic and transcriptional profiles of HY041 and HY037. The findings revealed that the genes encoding outer membrane protein A (OmpA), three peptidases, heat shock proteins, and proteins involved in lipopolysaccharide biosynthesis, and iron acquisition represent potential virulence factors of . . In conclusion, this study established . as a potential pathogen and identified significant differences in virulence across its strains, thereby enhancing our understanding of the pathogenesis of . .

, a fungal pathogen employed in pest biocontrol, can alkalize the surrounding environment, although the biological implications remain unclear. Here, we found that glutamate dehydrogenase 2 () was responsible for alkalization during fungal growth on insect wings or media containing cuticle powder. Loss of function resulted in significantly reduced virulence during both cuticle-passing and cuticle-bypassing infections but did not affect appressorium formation or cuticle penetration. Deletion of failed to alkalize amino acid-containing media under carbon deprivation, leading to impaired mycelia growth and conidiation. Hemolymph carbohydrates were decreased during infection, and the Δ mutant exhibited delayed fungal growth and impaired alkalization in hemolymph cultures. Notably, expression of , a pH-responsive transcription factor critical for virulence, was downregulated in hyphal bodies of the Δ mutant. Contrary to the established models in plant and human fungal pathogens, we demonstrate that Gdh2 activity is dispensable for appressorium formation but essential for fungal colonization in insect hemocoel during infection.

The species complex is one of the main etiological agents of cryptococcosis, a fungal infection that affects the lungs and progresses to meningoencephalitis. Neurological infections caused by this species are associated with a higher incidence of cryptococcoma, sequelae, and relapse. Despite its clinical relevance, the mechanisms that sustain the infection and persistence of in the central nervous system (CNS) are still poorly understood. In this study, we performed a comprehensive phenotypic characterization of the virulence of five strains, focusing on the CNS infectious biology. Significant differences in virulence among the strains were found, highlighting intracellular survival within macrophages and growth in the CNS as determining factors of disease severity. The relative capsule size between 1-2, as opposed to a marked increase (> 2), was associated with increased virulence, a phenomenon we term optimized capsule enlargement. Considering the high energetic cost of capsule synthesis, this pattern favors the fungal reproductive fitness and replication within the host's tissues. These findings indicate that, in addition to the ability to reach the CNS, needs to colonize it efficiently to cause severe clinical manifestations, with optimized capsule enlargement being a key factor for its survival in this microenvironment.

is a genus of apicomplexan parasites that causes diarrheal disease in humans and animals worldwide. The primary species affecting humans are and , while other species may also infect humans, specially immunocompromised individuals. Infections are particularly severe in people with weakened immune systems and malnourished children in developing countries. In livestock, especially young ruminants, leads to significant economic losses. The parasite occupies a unique epicellular niche and undergoes a complex life cycle involving both asexual and sexual stages. While the mechanisms of parasite invasion, replication, immune evasion, and tissue damage have been challenging to unravel due to earlier technical limitations and lack of genetic tools, recent advances have transformed our understanding. Innovations in genomics, transcriptomics, and molecular genetics have identified key virulence factors and clarified intricate host-parasite interactions. The parasite's secretory organelles (micronemes, rhoptries, dense granules, and small granules) play central roles by releasing molecules that facilitate host cell attachment, invasion, and modulation of host defenses. This review provides an up-to-date overview of the biology and pathogenic mechanisms of , highlighting structural features, invasion strategies, and host immune responses. It also covers recent progress in experimental models, vaccine development, and identification of new molecular targets for treatment and prevention. By synthesizing recent discoveries with previous research, this review offers a current perspective linking fundamental biology to disease outcomes and potential control strategies.

(), a prominent causative agent of mastitis in dairy cattle, remains enigmatic in its pathogenic mechanisms. This study aimed to reveal the effects of on mammary glands via the induction of ferroptosis, as well as the protective role of Ferrostatin-1 (Fer-1) against this pathogen-mediated damage in bovine mammary epithelial cells (BMECs). Holstein cows were used to establish an intramammary infection model of . , primary BMECs were treated with 10 μM Fer-1 and alone or in combination. The results showed that mammary glands infected with exhibited increased transcriptional levels of (), , , and (). Concurrently, significant elevations in iron, 4-hydroxynonenal, and reactive oxygen species (ROS) levels were observed. Conversely, infection downregulated nuclear factor erythroid 2-related factor 2 (Nrf2), cystine/glutamate antiporter (xCT), glutathione peroxidase 4 (GPX4), and glutathione levels. Following invasion, intracellular Fe and lipid ROS accumulated in the BMECs, impeding activation of Nrf2/xCT/GPX4 signal transduction. Additionally, Fer-1 facilitated the nuclear translocation of Nrf2 protein, upregulating the protein levels of Nrf2/xCT/GPX4 while downregulation transcriptional levels of , , , and . In conclusion, Fer-1 alleviates -induced inflammatory factor activation and ferroptosis in BMECs via upregulation of the Nrf2/xCT/GPX4 pathway, supporting ferroptosis inhibition holds promise as a feasible therapeutic agent for the control of mastitis.

RXLR effectors secreted by pathogens are important virulence factors in suppressing plant immunity and facilitating pathogen infection. In addition to possessing a variety of functions, some RXLR effectors have been found to trigger host cell death with different underlying mechanisms. was previously reported as a virulent RXLR effector secreted by and triggers cell death in various plants. However, it is uncertain whether this type of cell death promotes or restricts the colonization of this hemibiotrophic pathogen. Here, we explored the correlation between the cell death activity of and its contribution to the infection of . Sequencing data revealed that exhibited both point mutations and presence/absence polymorphisms in the population under positive selection. , one of four alleles, lost its cell death-inducing ability, also lost its ability to increase plant susceptibility to pathogen infection. Furthermore, could compromise the cell death-inducing and virulence functions of the other three alleles. truncated mutants deficient in cell death-inducing activity showed abolished ability to increase plant susceptibility. Finally, was unable to increase the susceptibility of TRV- plants, which showed abolished cell death. Taken together, the cell death-inducing activity of is essential for its virulence function during colonization of hemibiotrophic pathogen, suggesting that exploits the cell death triggered by to facilitate the transition from biotrophy to necrotrophy. These findings provide a new perspective for understanding the role of RXLR effectors triggered cell death in the pathogenesis of hemibiotrophic pathogens.

Flaviviruses are emerging pathogens, mostly transmitted by arthropod vectors, responsible for human, animal, and zoonotic diseases. The emergence of flaviviruses has been favored in recent decades by factors related to climate change and globalization, which contribute to the arrival and establishment of their vectors in new geographic areas, thus promoting epidemic outbreaks and facilitating these viruses to become endemic in these areas. This is the case of the West Nile virus (WNV) in Europe, which affects its natural bird host populations and also accidental hosts such as humans and horses. Flaviviruses are antigenically related, which induces cross-reactivity, making their serological diagnosis difficult, especially in areas where several flaviviruses co-circulate. Here, we have developed WNV biosensors in which the enzymatic activity of the viral protease, expressed during infection, allows its detection using fluorescence-based techniques. These biosensors carry WNV-specific protease cleavage sites and show high specificity for the detection of both lineages 1 and 2, with limits of detection (LODs) ranging from 0.001-0.0001 MOI at 48 hours post-infection (h.p.i.). These LODs are even lower at 72 h.p.i. reaching as low as an MOI of 2.5 × 10. They are also capable of detecting, although with lower sensitivity, other flaviviruses such as dengue, Zika, and Usutu viruses, without showing reactivity against unrelated viruses. These biosensors have been validated in viral neutralization assays with sera from infected mice and humans, as well as in antiviral screening, with results comparable to those of currently used systems, showing significant potential as clinical and laboratory tools.

Chronic persistent viral infections can lead to significant spleen damage, thus disrupting the host humoral immune response; however, the underlying mechanisms remain unclear. In this study, we employed a Lymphocytic choriomeningitis virus (LCMV) chronic infection model to investigate the effects of virus infection on spleen damage. Mice infected with Lymphocytic choriomeningitis virus clone 13 (LCMV-CL13) presented a series of pathological features, such as white pulp atrophy and reduced germinal center diameter, length, and area in the spleen. More importantly, we observed a diminished GC response alongside a weak antibody response in the chronic infection model. Single-cell RNA sequencing (scRNA-seq) further revealed the dysregulation of gene expression, including , , and , which inhibit B-cell differentiation during chronic viral infection. We verify that the upregulation of or , respectively, can promote apoptosis in BaF3 cells. Immune repertoire (IR) analysis revealed that the molecular diversity of the BCR repertoire after LCMV-CL13 infection, specifically manifested in BCR clonal diversity, gene segment usage preference, and CDR3 sequence changes. In conclusion, this study demonstrated that chronic LCMV-CL13 infection interrupted the development of splenic B cells by increasing the expression of apoptosis genes, thus enhancing our understanding of the underlying mechanisms of B-cell development interruption during chronic viral infection.

Bovine parainfluenza virus type 3 (BPIV-3) is a major pathogen associated with the bovine respiratory disease complex. However, the limited understanding of host factors crucial for BPIV-3 replication has hindered the development of effective preventive and therapeutic strategies. To tackle this critical issue, we constructed a bovine genome-wide CRISPR/Cas9 knockout library in Madin-Darby bovine kidney cells, which was then used to systematically identify and characterize the host genes essential for BPIV-3a replication. Subsequently, 10 genes were validated using both RT-qPCR and viral titration assays. Furthermore, through gene knockout or knockdown and rescue experiments, we identified three key genes required for BPIV-3a replication: Wnt family member 5A (WNT5A), solute carrier family 16 member 13 (SLC16A13), and selenoprotein N (SELENON). However, their effects on viral adhesion and internalization varied. WNT5A was involved in both processes, SLC16A13 participated solely in internalization, while SELENON had no significant impact on either. Beyond BPIV-3a, these three genes were also found to be essential for the infection of BPIV-3c and Bovine enterovirus. In conclusion, this study offers novel insights into the molecular mechanisms governing the replication and pathogenesis of BPIV-3a, BPIV-3c, and bovine enterovirus within host cells, thereby providing a foundation for identifying potential targets in the development of novel antiviral strategies.

Sepsis-induced cardiomyopathy (SICM) is a severe complication of sepsis, especially in children, and identification of novel therapeutic targets remains essential for improving patient outcomes. Recent studies have implicated N6-methyladenosine (mA), an RNA epigenetic modification, in SICM pathogenesis. However, the role of YTH domain-containing 2 (YTHDC2), an mA reader protein, in SICM remains unclear. This study used lipopolysaccharide (LPS)-treated adolescent rats, primary cardiomyocytes and H9c2 cardiomyocytes to mimic SICM and . We observed a significant upregulation of YTHDC2 and . Through comprehensive analyses including RNA sequencing (RNA-seq), Western blotting, and flow cytometry, we demonstrated that YTHDC2 promotes LPS-induced cardiomyocyte apoptosis. RNA immunoprecipitation sequencing (RIP-seq) and Western blotting further showed that YTHDC2 activates the LPS-induced NF-κB pathway. Mechanistic investigations using RIP-qPCR confirmed direct binding of YTHDC2 to mRNAs encoding the pro-apoptotic proteins BAX and BAK1, as well as the NF-κB subunit p65, with subsequent regulation of NF-κB transcriptional activity. Importantly, adeno-associated virus 9 (AAV9)-mediated cardiac-specific inhibition of YTHDC2 in adolescent rats effectively attenuated LPS-induced cardiomyocyte apoptosis and NF-κB pathway activation. Collectively, our findings establish YTHDC2 as a key regulator in SICM pathogenesis, promoting cardiomyocyte apoptosis and NF-κB signaling activation. These results highlight YTHDC2 as a promising therapeutic target for SICM.

Arthropod-borne viruses (arboviruses) pose significant public health threats, and understanding their evolutionary mechanisms can inform molecular diagnostics and vaccine design. Oropouche virus (OROV), a relatively understudied arbovirus, exhibits unique evolutionary dynamics in nucleotide composition. We analyzed 45 OROV strains across genotypes to assess selective pressures shaping nucleoprotein, glycoprotein, and RNA-dependent RNA polymerase (RdRp) evolution. We utilized information entropy, dinucleotide odds ratios, relative synonymous codon usage values, and context-dependent codon bias (CDCB) to elucidate the genetic characteristics associated with mono-, di-, tri-, and tetranucleotide compositions. The extent of overall nucleotide usage bias, dinucleotide bias, and synonymous codon usage bias did not correlate with genotype-specific patterns, but rather exhibited a protein function-dependent pattern across the three proteins. Although dinucleotide bias and synonymous codon usage bias varied within a relatively broad range, the dinucleotide CpG, the over- and under-represented synonymous codons, and CDCB remained strongly influenced by natural selective pressures from both the host and the viral life cycle. Furthermore, the codon usage patterns, as indicated by the effective number of codons, suggest that the OROV nucleoprotein has been subject to stronger selective pressures in its evolutionary paradigm compared to the glycoprotein and RdRp, which appear to be primarily influenced by natural selection and mutation pressure. Additionally, analysis of relative codon deoptimization index (RCDI) and tRNA adaptation index (tAI) revealed suboptimal translational efficiency of OROV coding sequences in human hosts, suggesting limited codon usage adaptation.

Human pathogenic fungi are ubiquitous in the environment and induce an expanding repertoire of devastating diseases globally. Upon fungal invasion, fungus adopt multiple strategies to adapt to, or eliminate, hostile environmental conditions, which immune checkpoints serve as one of the mechanism for fungal evasion. Programmed death receptor-1 (PD-1), an immunosuppressive molecule, transmits inhibitory signals upon binding to its ligand PD-L1. During infection, aberrant activation of the PD-1/PD-L1 pathway has been proven to facilitate immune evasion by the pathogen. In this review, we summarize the roles of PD-1/PD-L1 in fungal infection. First, the molecular structures and function of PD-1 and PD-L1 are described. Then, we highlight the dynamic expression patterns and regulatory mechanisms of PD-1/PD-L1 during fungal invasion. Potential therapeutics based on PD-1/PD-L1-blocking to enhance antifungal immunity and improve clinical outcomes are also discussed. These insights reveal future directions regarding PD-1/PD-L1 and immune checkpoint-based therapies for preventing pathogenic fungi infections.

Mitochondrial function is essential for virulence in , yet the mechanism by which mitochondria influence pathogenesis remains largely undefined. Here, we reveal that the mitochondrial-associated factor Mss2 controls invasive growth through the regulation of calcium-reactive oxygen species (ROS) homeostasis. Deletion of results in impaired invasive growth on solid media without affecting hyphal formation in liquid media, indicating that Mss2 controls contact-specific responses. We demonstrate that the regulation of these processes by Mss2 is linked to the regulation of cytosolic calcium levels and cellular ROS production. Furthermore, transcriptomic profiling identified -regulated genes, including , , , and , whose expression is dependent on calcium and ROS levels. Restoration of invasive phenotypes through exogenous ROS confirms the functional significance of this calcium-ROS circuit. In systemic infection models, similar to , the Mss2 downstream genes exhibit severe virulence defects. Together, this work is the first to show that mitochondrial regulation of a coordinated calcium-ROS circuit is required for invasive hyphal growth and virulence in . These findings refine our understanding of fungal invasion and virulence and reveal that targeting mitochondrial signaling could be an important area for antifungal therapeutic interventions.

The segmented nature and high mutability of the influenza virus RNA genome facilitate rapid mutation and reassortment, allowing the virus to breach host barriers and migrate between different species, potentially leading to unpredictable influenza outbreaks. With dogs emerging as new natural hosts for influenza virus, vigilant surveillance and scientific prevention strategies are imperative. Here, based on our previous isolation of 21 strains, which are reassortments of the canine influenza virus (CIV) H3N2 (KR/07) with gene segments from the influenza A pandemic (H1N1) 2009 virus strain (CA/09), the replication kinetics of these reassortants in immortalized mammalian respiratory epithelial cell lines from swine and ferret named hTERT-PBECs and hTERT-FBECs, alongside induced changes in cytokine expression, were investigated. Reverse genetics was utilized to generate the reassortment H3N2 canine influenza rKR/07-PB2/NP, which contains the PB2 and NP segments from CA/09. The viral titer of rKR/07-PB2/NP was significantly lower than those of the parental viruses KR/07 and CA/09. In addition, rKR/07-PB2/NP notably decreased expression levels of interleukin-1β (IL-1β) and interleukin-10 (IL-10) in both immortal cells, particularly in hTERT-PBECs. Our findings not only contribute to the understanding and exploring cross-species transmission mechanisms of influenza virus, but also provide new ideas for prevention and treatment of CIV.

The emerging cattle-adapted pathogen, Dublin, threatens the global cattle industry by causing high mortality in calves and reduced production efficiency in cows. Due to limited therapeutic options, there is a need for novel interventions to mitigate . Dublin. In the inflamed gut, Typhimurium, and possibly . Dublin, gain a metabolic advantage by utilizing niche nutrients during anaerobic respiration. . Dublin invades intestinal epithelial cells using genes encoded by Salmonella pathogenicity island 1 (SPI-1), initiating systemic disease and chronic infection. Propionate, a microbial fermentation product, inhibits SPI-1 transcription, presenting an opportunity to prevent infection. Lactobacilli endogenous to the small intestine of calves may be leveraged to inhibit . Dublin invasion and growth through propionate synthesis and nutrient blocking, respectively. Here, we discuss critical knowledge gaps of . Dublin pathogenesis while offering data-driven insights for the development of sustainable microbial-based interventions to mitigate . Dublin in cattle.

Hypervirulent (hvKp) presents challenges in infection management due to antibiotic resistance associated with its intracellular persistence. This study investigates the efficacy of phage therapy against intracellular hvKp using a two-stage murine model. We assessed changes in virulence, host survival, and immune responses through phagocytosis assays, transmission electron microscopy, and Western blotting, complemented by transcriptomic and proteomic analyses. Results indicate that phage therapy reduces mortality and modulates bacterial virulence by downregulating capsule production. Following phage exposure, hvKp adapts by enhancing its oxidative stress resistance. Crucially, these adaptations weaken host inflammatory and autophagy responses, enabling better survival within host cells. These adaptations suggest that while phage therapy can mitigate infection severity, the capacity of hvKp to modulate host pathways underscores the complexity of treating intracellular infections and highlights the importance of targeting both bacterial and cellular responses.

H11 subtype avian influenza viruses (AIVs) have been identified in both wild and domestic birds. H11N9 viruses from wild birds provided the NA gene to human H7N9 virus in 2013 in China, which caused five waves of human infections. During active surveillance in wild birds in China, 17 H11 viruses were isolated between December 2022 and January 2024, including six H11N1, one H11N2, one H11N3, and nine H11N9. The epidemiology of H11 subtype viruses in public databases revealed that they distributed across seven continents, and more than 54.9% of H11 viruses originated from wild Anseriformes. Phylogenetic analysis of the HA genes indicated that H11 viruses were classified into Eurasian and North American lineages, and our isolates belonged to the Eurasian lineage. Bayesian phylogeographic analysis suggested that Bangladesh served as a crucial geographical transmission center for H11 viruses in Eurasian lineage. Reassortment indicated that the H11 isolates in the study underwent complex genomic recombination with various subtype AIVs circulating in wild and domestic birds, including the clade 2.3.4.4b H5N1 highly pathogenic viruses, and formed seven genotypes. Notably, 17 H11 isolates acquired several mutations associated with enhanced human-type receptor binding in HA (S137A) and increased mammalian virulence in PB1 (D3V, D622G), PB1-F2 (N66S), M1 (N30D, I43M, T215A), and NS1 (P42S, I106M). Seven representative viruses exhibited dual receptor binding specificity and could infect mice directly without prior adaptation. These findings highlight the potential public health risks posed by H11 viruses from wild birds and emphasize the necessity of enhancing routine surveillance.

is an opportunistic fungal pathogen causing severe infections in immunocompromised individuals. Arginine metabolism is critical for immune regulation, but its precise role in cryptococcal pathogenesis is not well understood. In this study, we investigated systemic and tissue-specific alterations in L-arginine metabolism during pulmonary infection and evaluated L-arginine supplementation as a potential therapy using a murine model. Key assessments included fungal burden quantification, inflammatory cell and cytokine characterization, brain gene expression analysis, histological examinations, and survival studies. We found significant depletion of serum L-arginine and its downstream metabolites, accompanied by increased arginase activity in infected tissues, indicating a disrupted metabolic balance. Gene expression analysis showed distinct metabolic shifts, including upregulation of arginase-1 (Arg1) and proline metabolism genes, with concurrent suppression of nitric oxide synthase 2 (Nos2) in the brain during the late infection phase. Oral L-arginine supplementation significantly reduced fungal burdens in the brain and spleen, suggesting its effectiveness in controlling cryptococcal dissemination from the lungs. Consequently, L-arginine administration improved survival and clinical scores while also reducing brain cryptococcoma in infected mice. Mechanistically, L-arginine enhanced protective immune responses within the mouse brain, facilitated microglial-mediated clearance of , and reduced cryptococcal invasion across brain endothelial cells . In summary, oral administration of L-arginine mitigates dissemination by augmenting brain's immune response. This study provides crucial insights into arginine metabolism in cryptococcal disease progression, supporting L-arginine as a promising immunomodulatory therapy.

Gram-negative bacteria binding proteins (GNBPs) serve as essential pattern recognition receptors in insect innate immunity, detecting pathogen-associated molecular patterns to activate downstream immune responses. This molecular recognition mechanism presents a promising target for pest control strategies. However, the immunological functions of family members in remain poorly characterized, particularly for those with typical structural features. In this study, we identified and characterized a novel (designated ) from the cDNA library. Structural analysis revealed that TcGNBP3 exhibits the typical domain architecture characteristic of the family, comprising an N-terminal carbohydrate-binding module 39 (CBM39) domain and a C-terminal glycoside hydrolase family 16 (GH16) domain. Spatiotemporal expression profiling demonstrated peak transcript accumulation during the early pupal and late adult developmental stages, with predominant localization in immune-related tissues including the fat body and hemolymph. Bacterial challenges ( or ) induced significant upregulation of expression from 6 to 72 h. Molecular docking and ELISA analyses demonstrated TcGNBP3's binding affinity for lipopolysaccharide, peptidoglycan, and β-1,3-glucan, while functional assays confirmed its ability to bind and agglutinate five tested bacterial strains. RNAi-mediated silencing of severely compromised the beetles' immune response, suppressing immune-related genes (including transcription factors and antimicrobial peptides), disrupting prophenoloxidase cascade activation, and significantly reducing survival rates upon bacterial infection. These results identify as a key immune regulator in , supporting its development as an RNAi-based pest control target.

Since 2021, an epidemic disease characterized with hydrosalpinx fluid syndrome (HFS) has been circulating in the laying Sheldrake ducks in China, which seriously endangers the healthy development of the duck industry. The causative agent of this disease has been traced to avian metapneumovirus subtype C (aMPV/C), known to cause acute upper respiratory tract infections and egg-drop in poultry. To date, no reports have been made to isolate and characterize aMPV/C infection in Sheldrake ducks in China. Here, a strain of virus, designated aMPV-FJ21, was successfully isolated from the diseased ducks exhibiting HFS. Transmission electron microscopy revealed that the virus is an enveloped particle exhibiting a spherical or pleomorphic morphology. Indirect immunofluorescence assays demonstrated that the aMPV-FJ21 strain had an obvious reactive activity with the ploy-antibody against aMPV/C F protein. The complete genome of aMPV-FJ21 was determined to be 14,149 nucleotides in length. Notably, the amino acid sequence of the G protein was only 55.6%-78.7% identical to those of other aMPV/C reference strains. Phylogenetic analysis indicated that aMPV-FJ21 forms a distinct lineage within the aMPV/C group and is genetically distant from the North American and Eurasian lineages, suggesting that it may represent a novel genetic lineage. In challenge experiments, laying Sheldrake ducks with aMPV-FJ21 reproduced the typical clinical symptoms and pathological lesions observed in the field cases. Altogether, we had isolated a novel aMPV/C variant from Sheldrake ducks exhibiting HFS, distinct from previously reported strains, and provided the first evidence confirming its role as the causative agent of HFS in ducks.

Small extracellular vesicles (sEVs) play a role in the pathophysiology of viral respiratory infections, and may be suitable biomarkers for COVID-19 and Influenza infections or targets for treatment. We investigated differences in the surface proteome of plasma sEVs in patients with COVID-19 and Influenza.