Down-regulating CD19 surface markers expression correlates with infectious bursal disease virus replication.

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.

Tween 80 improves the infectivity of BCL1 cell-adapted infectious bursal disease virus.

Non-ionic surfactants have the ability to alter the cell membrane's permeability for enhancing virus replication. The impact of non-ionic surfactant Tween 80 (TW80) on the infectivity of infectious bursal disease virus (IBDV) was studied in BCL1 cells. The toxicity of different concentrations of TW80 for BCL1 cells was determined for five-time passages. The confluent monolayer of BCL1 was infected by IBDV and subsequently passaged. The adaptation was confirmed by virus titration and RT-PCR assay. Replication kinetics of the cell-adapted IBDV was evaluated in pre-treatment and simultaneous treatment with TW80 at 0.01% concentration. The IBDV infectivity patterns were determined by virus titration, FRAP assay, and transmission electron microscopy. Sequence analysis, RNA secondary structure, and potential N-glycosylation site were conducted for IBDV VP2. Despite the similar cytopathic effects found in both TW80-treated cells and similar ROS levels, the IBDV titer was higher in TW80 pre-treated cells compared to the simultaneous treatment one. Such an increase in IBDV titer did not associate with changes in the VP2 sequence and RNA secondary structure. The possible antioxidant capacity of TW80 can attenuate the ROS damage and improve the cell viability, thereby improving IBDV infectivity.