Shanshan Liu

Pseudorabies virus (PRV) is an immunosuppressive virus that causes significant damage to the pig industry. This study aimed to investigate the effects of PRV on oxidative stress and apoptotic related in the spleen of mice to provide basis knowledge for further research on the pathogenesis of PRV in mice model. 36 mice were randomly two groups, the control group which only received 200 μL PBS and infection group which was subcutaneously infected with 200 μL of 1 × 10³ TCID₅₀/100 μL PRV, respectively. Spleen tissues in each group were collected for further experiments at 48, 72, and 96 h post-infection (hpi). Pathological observation was performed by hematoxylin and eosin Y staining. Biochemical and Flow cytometry methods were used to determine the reactive oxygen species profile and apoptosis of the spleen post-infection and apoptosis detection. In addition, q-PCR and Western blot were adopted to measure the apoptotic conditions of the spleen infected with PRV. The results indicated that the reactive oxygen species (ROS) level in the PRV infection group was remarkedly increased (p < 0.01) at a time-dependent pattern. Furthermore, the Malondialdehyde levels in the spleen of mice in the infection group increased (p < 0.01) in a time-dependent mode. However, the activity of Catalase, Superoxide dismutase, and glutathione peroxidase and the content of Glutathione in the infection group were decreased with the control group (p < 0.01) at a time-dependent manner. In addition, the ratio of splenocyte apoptosis in the infection group significantly increased (p < 0.01) in a time-dependent manner. In conclusion, PRV infection causes apoptosis of the spleen via oxidative stress in mice.

Pseudorabies virus (PRV) is an immunosuppressive disease that causes significant damage to the pig industry. This study aimed to detect the effects of PRV on oxidative stress related factors and cell apoptosis in the spleen, providing a basis for the research on the pathogenesis of PRV in mice model. Pathological observation was performed by hematoxylin and eosin Y staining. Biochemical and Flow cytometry method were performed to determine the reactive oxygen species profile of the spleen post-infection and apoptosis detection. In addition, q-PCR and Western blot were adopted to measure the apoptotic conditions of the spleen infected with PRV. The results indicated that the ROS level in the PRV infection group was remarkedly increased ( p p p p p <0 01) in a time-dependent manner. In conclusion, PRV infection causes apoptosis of the spleen via oxidative stress in mice.

Ageratina adenophora is an invasive weed with widespread distribution. During the last several decades, many biologically active secondary metabolites have been isolated and characterized from A. adenophora, some of them having inspired the research and development of new therapeutic agents. This review mainly focuses on biological properties of A. adenophora, including the toxicity, antibacterial, antifungal, insecticidal, antiviral activities and others. In addition, the current limits and potentials of A. adenophora and its extracts are also discussed.

Pseudorabies (PR) is an acute infectious disease caused by pseudorabies virus (PRV). There are no available drugs due to the emergence of variant of PRV. Dihydromyricetin (DMY) is a flavonoid extracted from Ampelopsis grossedentata (A. grossedentata), which has a variety of pharmacological activities. In this study, we aim to investigate the in vitro anti-PRV activity of DMY extracted from A. grossedentata. MTT assay was used to detect the cytotoxicity and antiviral activity of DMY. The results detected by flow cytometry and qRT-PCR showed that DMY played anti-PRV role mainly by interfering with the process of virus invasion into host cell and inhibiting the occurrence of pyroptosis in vitro. This suggested that anti-pyroptosis may be an important antiviral mechanism for DMY which is expected to be a potential anti-PRV drug. Graphical Abstract

Pseudorabies virus (PRV), the causative agent of Aujeszky's disease, is one of the most harmful pathogens to the pig industry. PRV can infect and kill a variety of mammals. Nevertheless, the underlying pathogenesis related to PRV is still unclear. This study aims to investigate the pathogenesis induced by PRV in a mouse model. The mice infected with the PRV-HLJ strain developed severe clinical manifestations at 36 h post-infection (hpi), and mortality occurred within 48–72 hpi. Hematoxylin-eosin staining and qRT-PCR methods were used to detect the pathological damage and expression of cytokines related to an immune reaction in brain tissue, respectively. The cytokine storms caused by IFN-α, IFN-β, TNF-α, IL-1β, IL-6 and IL-18 were related to the histopathological changes induced by PRV. This pattern of cytokine secretion depicts an image of typical cytokine storms, characterized by dysregulated secretion of pro-inflammatory cytokines and imbalanced pro-inflammatory and anti-inflammatory responses. In addition, the pyroptosis pathway was also activated by PRV by elevating the expression levels of nod-like receptor protein 3, Caspase-1, Gasdermin-D and interleukin-1β/18. These findings provide a way for further understanding the molecular basis in PRV pathogenesis.