The changes of cell cycle progression and cellular signal transduction in Chinook salmon embryonic cells-214 after infectious pancreatic necrosis virus (IPNV-T42G) infection / 傳染性胰臟壞死病毒(IPNV-T42G)感染大眼鮭魚胚胎細胞株(CHSE-214)後細胞週期及訊息傳遞之變化

碩士 / 國立海洋大學 / 水產養殖學系 / 90 / Abstract
Infectious pancreatic necrosis virus (IPNV) belongs to the Birnaviridae family. It is currently one of the most serious infectious diseases in fish farming. Though IPNV was originally isolated as long as early 1960s, little is known about the mechanism related to the viral induced intracellular molecular changes that support viral replication.
In this thesis we try to assess the cell cycle progression of the infected cells and to assess the potential role of cellular signal transduction in
IPNV replication.
Infection of cells by many viruses affects the cell division cycle of their host cells to favor viral replication. The cell cycle progression was performed by flow cytometry analysis, when CHSE-214 cells synchronized by growth inhibition were infected with IPNV. IPNV infected cells were arrested in the a G0/G1 phase at 3h after infection (78.3% of the cells in the G0/G1 phase, 12.4% in the S phase, and 9.17% in the G2/M phase). The result indicats that IPNV prevent normal cell cycle progression of CHSE-214 and the event is triggered early after virus infection by specific interaction with cellular components that regulate cell cycle progression.
A variety of DNA and RNA viruses induce signaling through MAP kinase family cascades in infected cells. The Western blot analysis of the phosphorylated protein was performed in CHSE-214 cells absorbed purified IPNV which was UV irradiated or untreated when cells were starved by the medium with no serum. ERK and CREB were phosphorylated in CHSE-214 after IPNV or UV-irradiated IPNV absorption, while JNK and p38 were dephosphorylated. However, IPNV absorption did not affect the activity of IκBα, an inhibitor of transcription factor NF-κB. The results indicate that IPNV initiates a signaling pathway without viral gene products and viral gene products may lead to the second time kinase activation.

Identiferoai:union.ndltd.org:TW/090NTOU0086002
Date January 2002
Creators李盈撰
Contributors, 林正輝, 徐亞莉
Source SetsNational Digital Library of Theses and Dissertations in Taiwan
Languagezh-TW
Detected LanguageEnglish
Type學位論文 ; thesis
Format0

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