Dexamethasone treatment decreases replication of viral hemorrhagic septicemia virus in Epithelioma papulosum cyprini cells

被引:4
|
作者
Kim, Min Sun [1 ]
Lee, Su Jin [2 ]
Choi, Seung Hyuk [3 ]
Kang, Yue Jai [4 ]
Kim, Ki Hong [3 ]
机构
[1] Sejong Univ, Grad Sch Integrated Bioind, Seoul 05006, South Korea
[2] Natl Fishery Prod Qual Management Serv, Incheon Airport Reg Off, Incheon, South Korea
[3] Pukyong Natl Univ, Dept Aquat Life Med, Busan 48513, South Korea
[4] Sun Moon Univ, Dept Aquat Life & Med Sci, Asan 31460, Chungnam, South Korea
关键词
Dexamethasone; VHSV; Replication; Type I IFN; HSP90; MAMMARY-TUMOR VIRUS; SALMON SALMO-SALAR; RAINBOW-TROUT; MARINE FISH; INCREASES SUSCEPTIBILITY; GLUCOCORTICOID-RECEPTOR; INTERFERON RESPONSE; IMMUNE-RESPONSES; HSP90; INFECTIONS;
D O I
10.1007/s00705-017-3248-x
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The expression of Mx1 in EPC cells after treatment with poly(I:C) or infection with viral hemorrhagic septicemia virus (VHSV) was significantly suppressed by treatment with dexamethasone. However, the titer of VHSV did not increase but instead decreased after dexamethasone treatment. This suggests that dexamethasone not only downregulates type I IFN but also affects certain factors that are necessary for VHSV replication. An important effect of HSP90 on replication of RNA viruses and downregulation of HSP90 by glucocorticoids have been reported. In this study, dexamethasone downregulated HSP90 alpha expression in EPC cells that were stimulated with poly(I:C) or infected with VHSV. Furthermore, cells treated with an HSP90 inhibitor, geldanamycin, showed significantly decreased titers of VHSV, suggesting that HSP90 may be an important host component involved in VHSV replication, and HSP90 inhibition might be one of the causes for the observed reduction in viral titer caused by dexamethasone treatment.
引用
收藏
页码:1387 / 1392
页数:6
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