DPV UL38 stabilizes MFN2 to subvert MAVS-mediated antiviral immunity in ducks.

Duck plague is a highly contagious disease caused by duck plague virus (DPV) infection, leading to high morbidity (up to 100 %) and mortality rates (up to 95 %) among ducks. Mitochondria are essential organelles for virus replication. It is crucial to deepen the understanding of mitochondrial homeostasis and the interaction between mitochondrial proteins after viral infection.

sp. nov., isolated from the upper respiratory tract of duck.

Five bacterial strains, designated as RCAD1438, RCAD1439, RCAD1670, RCAD1671 and RCAD1672, were isolated from the upper respiratory tract of ducks in Anhui, Shaanxi and Sichuan, China. All strains are Gram-stain-negative, rod-shaped, non-motile, non-spore-forming, aerobic and capsulated. They grow optimally at 37 °C and pH 7.

Duck plague virus ICP27 protein suppresses IFN-β production by dual targeting of DNA- and RNA-sensing pathways.

Duck plague virus (DPV), an alphaherpesvirus causing severe economic losses in global waterfowl industries, adopts sophisticated strategies to subvert host antiviral immunity. Here, we identify DPV ICP27 as a pivotal immune evasion protein that concurrently inhibits both DNA (cGAS-STING) and RNA (RIG-I/MDA5-MAVS) innate immune sensing pathways-a novel function unreported in avian herpesviruses. Through co-transfection and infection assays in duck embryo fibroblasts (DEFs), we demonstrate that ICP27 suppresses key immune sensors' transcriptional and protein expression levels (STING, RIG-I) and the transcription factor IRF7.

The duck plague virus UL7 protein mediates RIG-I degradation to block host antiviral responses and promote viral pathogenesis.

Duck plague (DP), which is caused by duck plague virus (DPV), is an acute, highly contagious disease with an extremely high mortality rate, and poses a serious threat to the waterfowl industry. DPV, which is an immunosuppressive virus, can significantly suppress host innate immune responses during the late stages of infection. However, the specific mechanisms by which the DPV UL7 protein functions in the viral replication cycle and immune evasion remain unclear.

Roles of SPI-2 T3SS effectors in virulence of Choleraesuis and Construction of a triple-gene mutant vaccine strain.

Effector protein functions of Type III secretion system (T3SS) encoded by pathogenicity islands 2 (SPI-2) have not been fully characterized in serovar Choleraesuis. This study characterized 21 effectors of SPI-2 T3SS of in terms of macrophage survival and virulence in mice via construction of various gene mutant strains. Eight effector genes including , , and contributed to bacterial survival in macrophage cell line RAW264.

Deciphering pUL10's mastery in duck plague virus virulence: dual coordination of host immunity and viral replication.

Interferon (IFN) critically regulates antiviral immunity, wherein its production level determines disease progression, many viruses disrupt these defenses through mechanisms that remain incompletely understood. This study investigates the effect of duck plague virus (DPV) infection on immune organs and elucidates the molecular mechanism by which its UL10 protein (pUL10) inhibits melanoma differentiation-associated protein 5 (MDA5)-mediated IFN-β production. DPV UL10 gene encodes pUL10, a virulence-associated protein critical for viral pathogenicity.

Two receptor-targeting mechanisms of lambda-like siphophage Gifsy-1 of Salmonella Typhimurium.

The receptor-targeting mechanisms by which λ-like siphophages establish infection in gram-negative bacteria remain poorly characterized. This study demonstrated that the λ-like phage Gifsy-1, which exhibits broad lytic activity in Salmonella enterica, employs two receptor-targeting mechanisms mediated by the side tail fiber Stf and central tail tip J dependent on O-polysaccharide (OPS) production. In rough (OPS-deficient LPS) Salmonella Typhimurium strains, Gifsy-1 employs multiple receptor-targeting: the J protein binds OmpC, OmpX, and BtuB, while the Stf protein targets galactose II (Gal II) of the lipopolysaccharide (LPS) core oligosaccharide.

The chaperone DnaK promotes the emergence and accumulation of antibiotic-resistant clones through its ATPase activity in Riemerella anatipestifer.

The rapid emergence of antibiotic-resistant bacteria has become a global concern. In particular, the overuse of antibiotics in the breeding industry has accelerated the emergence of antibiotic-resistant bacteria, but the mechanisms driving this phenomenon are not fully understood. Here, using the multidrug-resistant bacterium R.

The Protein Encoded by the UL3.5 Gene of the Duck Plague Virus Affects Viral Secondary Envelopment, Release, and Cell-to-Cell Spread.

Duck plague (DP), caused by duck plague virus (DPV), is a highly contagious and fatal disease among waterfowl. UL3.5, an unconserved gene belonging to the family, subfamily, and genus, is located downstream of UL3 and exhibits high variability in size and sequence, with an absence in herpes simplex virus (HSV).

Cooperative nuclear import of duck plague virus DNA polymerase subunits: pUL42 NLS Enhances pUL30 nuclear import and viral replication, with VP22 as a compensatory factor.

Duck plague (DP), caused by duck plague virus (DPV), is an acute, febrile, and septic disease fatal to geese, ducks, and other wild waterfowl. The DPV UL42 gene product, pUL42, an accessory subunit of the viral DNA polymerase, whose nuclear import is critical for viral replication; however, the underlying mechanism remains unclear. In this study, we identified a 33-amino acids region at the C-terminus of pUL42, containing its nuclear localization signal (NLS).

High prevalence of Duck Hepatitis B virus-associated coinfection in Southwest China.

Currently, five types of duck hepatitis viruses have been documented, and they are all associated with liver disorders. However, the prevalence of their coinfections involving these viruses remains largely uncertain. Herein, we screened the prevalence of the five types of hepatitis viruses from A to E in 143 samples of diseased duck livers during 2019-2021 in Southwest China.

Duck plague virus gG is secreted, nonstructural glycoprotein, not essential for viral replication and responsible for the virulence.

Duck plague virus (DPV) is a highly pathogenic member of the herpesvirus family that can induce significant morbidity and mortality, primarily manifesting as septicemia in multiple host organs. The US4 gene encodes glycoprotein gG, which is highly conserved across the alphaherpesvirus family. To date, our laboratory has conducted preliminary bioinformatics analysis and prokaryotic expression studies of DPV US4; however, there is a paucity of literature regarding its biological characteristics and functions.

Functional characterization of the chaperone DnaK of Riemerella anatipestifer in antibiotic resistance and pathogenicity.

Antibiotic resistance has become a global public health problem, which is closely related to humans, animals and the environment. Riemerella anatipestifer (R. anatipestifer, RA) is a Gram-negative, multi-resistant bacterium that infects ducks and other birds.

Identification and Characterization of Linear Epitopes of Monoclonal Antibodies Against the Capsid Protein of Goose Astrovirus Genotype 2.

Since 2015, outbreaks of a disease causing severe visceral gout in goslings had resulted in substantial economic losses to the goose farming industry in China. Subsequently, the disease, characterized by extensive visceral urate deposition and renal swelling, was determined to be caused by a novel astrovirus, designated as goose astrovirus (GAstV). The capsid protein (Cap) of GAstV, encoded by ORF2, is the sole structural protein of the virus and holds potential for developing therapeutic antibodies and diagnostic tools.

A RT-ERA-CRISPR/Cas12a assay for rapid point-of-care duck hepatitis A virus detection.

Duck hepatitis A virus (DHAV) is a severe pathogen that threatens the duck industry. DHAV is transmitted primarily through the respiratory and gastrointestinal tracts. Therefore, developing accurate and rapid diagnostic technologies is crucial to prevent the spread of this infectious disease.

Duck plague virus US3 kinase phosphorylates and induces STING degradation to inhibit innate immune responses.

Duck plague virus (DPV) causes the highest mortality rate among aquatic birds; however, its antago nistic mechanism against antiviral innate immune responses remains elusive. In this study, we systematically screened and found that most DPV genes have inhibitory potential for duck cyclic guanosine monophosphate-adenosine monophosphate synthetase (cGAS)/stimulator of interferon (IFN) gene (STING) pathway-mediated antiviral responses, with the DPV US3 kinase showing the strongest inhibitory activity. Co-immunoprecipitation and immunoblotting assays demonstrated that DPV US3 interacted with STING and induced its degradation.

An efficient bivalent vaccine against duck Tembusu and duck plague viruses based on ribosomal skipping of DHAV-1 2A1 and abundant expression of DPV protein.

Duck Tembusu virus (DTMUV) and duck plague virus (DPV) are common duck pathogens that cause significant annual economic losses to the poultry industry. In this study, a recombinant virus DPV-(UL49-2A1-E) expressing the DTMUV E protein was successfully constructed and evaluated for its immunological effects using a duck-derived viral protein with ribosome jumping function, duck hepatitis A virus type 1 (DHAV-1) 2A1, to ligate a DTMUV -truncated E protein positioned before the termination codon of the DPV high-abundance expression protein pUL49. Immunofluorescence and western blot analyses revealed that the E protein was normally expressed in DPV-(UL49-2A1-E)-infected duck embryo fibroblasts.

The A487 residue in the E protein of duck Tembusu virus significantly enhances viral replication and increases its neurovirulence in Kunming mice.

Unlabelled: Tembusu virus (TMUV), an emerging avian orthoflavivirus, causes severe egg-drop syndrome and encephalitis in ducks. Although ducks are the natural host, mice serve as a valuable model for studying neuropathogenesis, as TMUV-infected mice recapitulate key neurological symptoms observed in ducks, such as paralysis and encephalitis. In the previous study, we observed that the TMUV strain CQW1 exhibited unexpectedly low neurovirulence in mice compared with earlier strains, highlighting potential genetic determinants of pathogenicity that may influence viral evolution and disease outcomes in natural hosts.

The Third Conserved Cysteine Residue in the Zinc-Binding Domain of Duck Plague Virus ICP8 Is Responsible for Its Single-Stranded DNA-Binding Ability, Viral Attenuation and Protection Against Lethal Challenge.

The innovative genetically engineered vaccinations can address the drawbacks of traditional vaccines, including atavism, virulence return, and risk of virus transmission, which are essential for limiting the spread of duck plague and ultimately eradicating it. ICP8 is the only single-stranded DNA-binding protein (SSB) of herpesviruses and is required for viral DNA replication, making it an excellent target for research into the pathogenicity of the duck plague virus (DPV) and the development of vaccines. In this research, we generated three ICP8 mutant proteins and corresponding mutant viruses to assess their contribution to single-stranded DNA (ssDNA) binding ability, pathogenicity, and vaccine potential in vitro and in vivo.

A noninfectious pseudovirus system for an emerging orthoflavivirus.

• A -complementation system for Usutu virus (USUV) recapitulates authentic viral replication. • High yield of TMN-ΔNS1 virus was obtained with no recombination into replication competent viruses. • TMN-ΔNS1 can be -complemented by heterologous orthoflavivirus NS1.

Genomic analysis of Proteus mirabilis: Unraveling global epidemiology and antimicrobial resistance dissemination - emerging challenges for public health and biosecurity.

Given the escalating public health threat posed byProteus mirabilis(P. mirabilis) and its rapidly evolving drug resistance, it is imperative to elucidate its global epidemiology and resistance mechanisms through a comprehensive genomic lens. As of August 2024, 3,403 high-qualityP.

High prevalence of plasmid-mediated Fosfomycin resistance in waterfowl-derived strains: insights into genetic context and transmission dynamics in China.

Fosfomycin (FOS) is a critical antibiotic for treating multi-drug resistant (MDR) infections, but its effectiveness is jeopardized by the dissemination of plasmids encoding enzymes that modify FOS. Despite the prohibition on its use in animal breeding in China, 100 strains of () exhibiting high resistance to FOS (MIC≥512 mg/L) were isolated from samples of waterfowl origin collected in Hainan, Sichuan, and Anhui. These strains commonly carried the A (88/100, 88.

Emergence of multidrug resistant Escherichia coli coharboring fosA3 and ESBL genes from retail ducks along slaughter line.

The excessive and indiscriminate use of antimicrobial agents in poultry production has increased antimicrobial resistance in E. coli, posing a significant threat to public health. This study investigated the prevalence of multidrug-resistant (MDR) E.

Unique long 11 and 16 protein act as a bridge for the unique long 11, 16, 21 protein and glycoprotein E interaction in duck plague virus replication.

Unique long (UL) 11, 16, and 21 proteins are duck plague virus (DPV) tegument proteins that are important in virus replication and cell-to-cell spread. gE is an envelope glycoprotein that is critical for DPV virulence. However, information regarding the interactions among DPV viral proteins is limited.

Duck plague virus UL47 gene affects the release and cell-to-cell spread of the virus and its deletion strains can provide strong protection for ducks.

Duck plague (DP) is an acute, febrile, septicemic infectious disease caused by duck plague virus (DPV). pUL47, which is encoded by the DPV UL47 gene, is a relatively abundant late tegument protein in virions, and its effects on the life cycle and virulence of viruses remain unclear. Herein, we generated UL47-deficient DPVs through a two-step Red recombination system and examined the effects of UL47 on the viral life cycle, virulence, and immune protection of UL47-deficient strains.