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United States Department of Agriculture

Agricultural Research Service

Research Project: CATFISH GENETICS, BREEDING, AND PHYSIOLOGY Title: Poly I:c Inhibits the Expression of Channel Catfish Virus Immediate-Early Gene Orf 1 at Early Times after Infection

Authors
item Silverstein, Peter
item Li, Robert
item Murdock, Christopher
item Waldbieser, Geoffrey

Submitted to: Fish and Shellfish Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 8, 2006
Publication Date: August 1, 2007
Citation: Silverstein, P.S., Li, R.W., Murdock, C.A., Waldbieser, G.C. 2007. Poly i:c inhibits the expression of channel catfish virus immediate-early gene orf 1 at early times after infection. Fish and Shellfish Immunology 23:479-484.

Interpretive Summary: Channel catfish virus (CCV) is a herpes virus that infects channel catfish fry and fingerlings. Previous research has demonstrated that genes involved in the host immune response can inhibit the expression of genes that are critical for the replication of some mammalian herpesviruses. Both the virus, and the host immune response that the virus will encounter, are greatly diverged from their mammalian counterparts. In this work we demonstrate that at least one mechanism of host inhibition of the virus appears to be conserved. If this model holds true for other CCV-host immune interactions, it could impact the effect of CCV on the outcome of infection with other pathogens (e.g. bacterial or fungal pathogens).

Technical Abstract: Channel catfish virus (CCV) is a herpes virus that infects channel catfish fry and fingerlings. Previous research has demonstrated that Type I interferons inhibit the expression of immediate-early (IE) genes of some mammalian herpesviruses. However, CCV is distantly related to the mammalian herpesviruses and Type I interferons from higher vertebrates exhibit only 20% similarity to fish interferons. In this work we demonstrate that treatment of channel catfish ovary (CCO) cells, a fibroblast-like cell line, with poly I:C, a known inducer of Type I interferons, results in inhibition of expression of the CCV IE gene ORF 1. Thus, although the genes involved have diverged, the mechanism appears to be conserved. If this paradigm holds true for other CCV IE-Type I interferon interactions, it could have important implications for the impact of CCV on the host immune system.

Last Modified: 10/24/2014
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