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Infectious bursal disease virus (IBDV) caused an acute and highly contagious infectious disease characterized by severe immunosuppression, causing considerable economic losses to the poultry industry globally. Although this disease was well-controlled under the widely use of commercial vaccines in the past decades, the novel variant IBDV strains emerged recently because of the highly immunized-selection pressure in the field, posting new threats to poultry industry. Here, we reported novel variant IBDV is responsible for a disease outbreak, and assessed the epidemic and pathogenicity of IBDV in this study. Moreover, we constructed a challenge model using Fowl adenovirus serotype 4 (FAdV-4) to study on the immunosuppressive effect. Our findings underscore the importance of IBDV surveillance, and provide evidence for understanding the pathogenicity of IBDV., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

MicroRNAs (miRNAs) involved host-virus interaction, affecting the replication or pathogenesis of several viruses. Frontier evidences suggested that miRNAs play essential roles in infectious bursal disease virus (IBDV) replication. However, the biological function of miRNAs and the underlying molecular mechanisms are still unclear. Here, we reported that gga-miR-20b-5p acted as a negative factor affecting IBDV infection. We found that gga-miR-20b-5p was significantly up-regulated during IBDV infection in host cells, and that gga-miR-20b-5p effectively inhibited IBDV replication via targeting the expression of host protein netrin 4 (NTN4). In contrast, inhibition of endogenous miR-20b-5p markedly facilitated viral replication associated with enhancing NTN4 expression. Collectively, these findings highlight a crucial role of gga-miR-20b-5p in IBDV replication., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Autophagy is a conserved process by which cells maintain homeostasis. However, abnormalities in autophagy can lead to the development of various diseases, including cancer. Avian leukosis virus Subgroup J (ALV-J) is an oncogenic exogenous retrovirus, which induces severe immunosuppression and development of tumors in susceptible host. This study reveals for the first time that ALV-J inhibits autophagy through the envelope protein gp37. Here we demonstrate that envelope protein gp37 blocks the fusion of autophagosomes to lysosomes and induces incomplete autophagy. Interestingly, additional experiments revealed that the host chaperone protein TCP1 is also an autophagy inhibitor and blocking the process of autophagic flow in DF-1 cells. Through immunoprecipitation assays, we found that TCP1 interacts with gp37. In addition, TCP1 knockdown also abolished gp37-mediated inhibition of autophagy in DF-1 cells. Furthermore, TCP1 mediates gp37 of ALV-J to inhibit autophagy through activating AKT for promoting viral replication in DF-1 cells., (Copyright © 2022 Elsevier B.V. All rights reserved.)

MicroRNAs (miRNAs) involved host-virus interaction, affecting the replication or pathogenesis of several viruses. Although avian leukosis virus subgroup J (ALV-J) has been one of the most studied avian viruses, the effects of various host miRNAs on ALV-J infection and its underlying molecular mechanisms are still unclear. Here, we reported that gga-miR-200b-3p acts as a positive host factor enhancing ALV-J replication. We found that gga-miR-200b-3p was increased in response to ALV-J infection in host cells, and that gga-miR-200b-3p effectively enhanced ALV-J replication via targeting host protein dual-specificity phosphatase 1 (DUSP1). Collectively, these findings highlight a crucial role of gga-miR-200b-3p in ALV-J replication., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Control of ALV-J in breed of chicken is still a serious issue that need more attention to be paid. Vertical transmission of ALV-J often give rise to more adverse pathogenicity. However, the way to elimination of ALV-J underlying vertical transmission remains not-well understood. In addition, effective vaccines or drugs have not been developed to prevent and control the transmission of ALV-J so far. CD81, a member of the tetraspanins superfamily, plays important roles in regulating membrane proteins, facilitating cells adhesion or fusion, and also participates in viral infection. The purpose of this study was to investigate whether antibodies against certain tetraspanins affect infection of ALV-J. Here, we showed that anti-CD81 antibody could inhibit viral RNA and protein level. We also found that anti-CD81 antibody interacts with viral protein p27, p32 and gp37. Moreover, treatment with antibody to CD81 can effectively prevent the vertical transmission of ALV-J in animal model. Collectively, current study provides new avenues for the control of ALV-J transmission., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Pseudorabies virus (PRV) is a zoonotic agent with a wide host range, causing significant economic losses in animal husbandry and potential public health risk globally. The causative agent has recently gained attention due to the inter-species transmission among different species of animals, even human beings. Although PRV's prevalence is found in many species of animals, regardless of whether the strain involved is a vaccine, classical or variant, few lines of evidence for the viral transmission route are available. Here, we reported that viral contamination is associated with the inter-species transmission of PRV. We found that PRV contamination was widely distributed in the environment of pig farms, that viral distribution in the environment is associated with the implementation of biosecurity measures, and that PRV could transmit from pigs to dogs through virally contaminated fomites. Collectively, our findings provide a basis for understanding the ecology and transmission route of PRV and underscore the importance of implementing biosecurity measures to control this disease., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Pseudorabies virus (PRV) is considered as an infectious agent with a wide of host range, causing considerable economic losses in animal husbandry. Although the commercial vaccine against PRV plays an critical role in control of this disease in swine industry, the potential risk of commercial vaccines against PRV for other host is unclear. Here, we report that the commercial vaccine against PRV is a hidden health risk for dogs. We found that different attenuated PRV strains in commercial vaccines possess different tissue tropism, and that the attenuated PRV strains are lethal to dogs, and that the attenuated PRV strain possesses the ability to spread horizontally among the dogs. Collectively, our findings provide clues that the commercial vaccine against PRV is a hidden risk for dogs, even for the owner of pet dogs to take seriously., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Porcine parvovirus (PPV) is a major causative agent of reproductive failure in swine, which currently affects the swine industry worldwide. Although PPV was identified several years ago, little is known about how it overcomes host innate immunity. In this study, we used quantitative real-time PCR and a luciferase reporter assay to determine whether PPV infection induces type I interferon (IFN-α and IFN-β) and whether PPV infection blocks dsRNA-induced IFN-β promoter activation in cell cultures. The results indicate that PPV does not induce type I interferon and that the NS2 protein of PPV could blocks dsRNA-induced IFN-β promoter activation., (Copyright © 2012 Elsevier B.V. All rights reserved.)