Search

The infectious bursal disease virus (IBDV) causes an acute and highly contagious immunosuppressive response in young chickens by targeting B lymphocytes in immune organs. Changes in regulatory T-cell ratio and apoptosis have been demonstrated during IBDV infection in these cells. The possible change in CD19 expression as the precursor of B cells after IBDV replication was detected in this study. Raji cells were infected with an IBDV isolate at MOIs of 1.0 and 3.0. The viral kinetics were determined using the characteristic virus-induced CPE, cell viability, and infectious titer. Induction of apoptosis and also changes in the CD19 expression within the virus infection were assessed by flow cytometry. The Raji cells were found to be susceptible to IBDV infection by producing marked CPEs dependent on MOI. The infectivity titers were determined in intra- and extracellular samples at the defined hours. The kinetics of early IBDV replication in Raji cells were nearly identical for both MOIs, but a significant difference in the infectivity titer was observed at 48 hpi. The quick apoptotic events were observed to be significantly higher in MOI 3.0, which was correlated with the lower virus titer. A significant CD19 expression change in the IBDV-infected Raji cells was revealed. The results suggested that Raji cells mimic the IBDV replication in lymphoid organs and the virus replication is related to CD19 expression frequencies in the lymphoid cells. • IBDV targets the medullary bursa in the avian host with a preference for B cells. • Raji cell line has the potential for IBDV replication and support higher viral growth titers. • Changes in Bregs expression be suitable in monitoring IBDV replication in a B cell-originated cell line. • The change in the level of CD19 marker is closely associated with IBDV infection. [ABSTRACT FROM AUTHOR]

Epilepsy is a common neurological disorder that significantly affects the quality of life of patients. In this study, we aim to evaluate the effectiveness of dental pulp stem cell (DPSC) transplantation in decreasing inflammation and cell death in brain cells, thus reducing seizure damage. We induced seizures in rats using intraperitoneal injections of pentylenetetrazole (PTZ). In the PTZ + DPSC group, we conducted bilateral hippocampal transplantation of DPSCs in PTZ-lesioned rat models. After 1 month, we performed post-graft analysis and measured some behavioral factors, such as working memory and long-term memory, using a T-maze test and passive avoidance test, respectively. We investigated the immunohistopathology and distribution of astrocyte cells through light microscopy and Sholl analysis. Additionally, we employed the Voronoi tessellation method to estimate the spatial distribution of the cells in the hippocampus. Compared to the control group, we observed a reduction in astrogliosis, astrocyte process length, the number of branches, and intersections distal to the soma in the hippocampus of the PTZ + DPSC group. Further analysis indicated that the grafted DPSCs decreased the expression of caspase-3 in the hippocampus of rats with induced seizures. Moreover, the DPSCs transplant protected hippocampal pyramidal neurons against PTZ toxicity and improved the spatial distribution of the hippocampal neurons. Our findings suggest that DPSCs transplant can be an effective modifier of astrocyte reactivation and inflammatory responses. [ABSTRACT FROM AUTHOR]

Chemoresistance is often referred to as a major leading reason for cancer therapy failure, causing cancer relapse and further metastasis. As a result, an urgent need has been raised to reach a full comprehension of chemoresistance-associated molecular pathways, thereby designing new therapy methods. Many of metastatic tumor masses are found to be related with a viral cause. Although combined therapy is perceived as the model role therapy in such cases, chemoresistant features, which is more common in viral carcinogenesis, often get into way of this kind of therapy, minimizing the chance of survival. Some investigations indicate that the infecting virus dominates other leading factors, i.e., genetic alternations and tumor microenvironment, in development of cancer cell chemoresistance. Herein, we have gathered the available evidence on the mechanisms under which oncogenic viruses cause drug-resistance in chemotherapy. [Display omitted] [ABSTRACT FROM AUTHOR]