Transcriptomic analysis of the host response to early stage salmonid alphavirus (SAV-1) infection in Atlantic salmon Salmo salar L.
- 作者：Tharangani K. Herath ; t.k.herath@stir.ac.uk ; James E. Bron ; Kim D. Thompson ; John B. Taggart ; Alexandra Adams ; Jacqueline H. Ireland ; Randolph H. Richards
- 关键词：Transcriptomic analysis ; Host response ; Salmonid alphavirus-1 (SAV-1) ; Atlantic salmon
- 刊名：Fish & Shellfish Immunology
- 出版年：2012
- 期刊代码：115_10504648
- 类别：abs
- 出版时间：May, 2012
- 卷：32
- 期：5
- 页码：796-807
- 文件大小：1656 K
摘要
Salmon pancreas disease, caused by salmonid alphavirus (SAV) of the family Togaviridae, is an economically important disease affecting farmed Atlantic salmon (Salmo salar L.) in Scotland, Norway, and Ireland. The virus causes characteristic lesions in the pancreas, heart, kidney and skeletal muscle of infected fish. The mechanisms responsible for the pathology and the immune responses elicited in infected Atlantic salmon are not fully understood. A microarray-based study was therefore performed to evaluate the host transcriptomic response during the early stages of an experimentally-induced SAV-1 infection. Atlantic salmon parr were injected intra-peritoneally with viral cell culture supernatant or cell culture supernatant without virus. RNA, extracted from head kidney sampled from infected and control fish at 1, 3 and 5 days post-injection (d.p.i.), was interrogated with the 17聽k TRAITS/SGP cDNA microarray. The greatest number of significantly differentially expressed genes was recorded at 3聽d.p.i., mainly associated with immune and defence mechanisms, including genes involved in interferon I pathways and Major Histocompatibility Complex Class I and II responses. Genes associated with apoptosis and cellular stress were also found to be differentially expressed between infected and uninfected individuals, as were genes involved in inhibiting viral attachment and replication. The microarray results were validated by follow-on analysis of eight genes by real-time PCR. The findings of the study reflect mechanisms used by the host to protect itself during the early stages of SAV-1 infection. In particular, there was evidence of rapid induction of interferon-mediated responses similar to those seen during mammalian alphavirus infections, and also early involvement of an adaptive immune response. This study provides essential knowledge to assist in the development of effective control and management strategies for SAV-1 infection.