1. Tween 80 improves the infectivity of BCL1 cell-adapted infectious bursal disease virus.
- Author
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Shahsavandi, Shahla, Ebrahimi, Mohammad Majid, Ghadiri, Mohammad Bagher, and Samiee, Mohammad Reza
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INFECTIOUS bursal disease virus , *TITERS , *NONIONIC surfactants , *TRANSMISSION electron microscopy , *MEMBRANE permeability (Biology) , *SEQUENCE analysis , *VIRAL replication - Abstract
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. • Infectious bursal disease virus isolate adapts to BCL1 cells following five subsequent passages. • The low concentration of non-ionic surfactant Tween 80 supports IBDV replication to high titers. • A high correlation estimates between the antioxidant activity and the replication of virus. • A synonymous substitution at 1019 nucleotide of VP2 detects as a silent mutation. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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