Shrimp SIRT1 activates of the WSSV IE1 promoter independently of the NF-κB binding site.

Since the mechanisms by which cellular factors modulate replication of the shrimp viral pathogen white spot syndrome virus (WSSV) are still largely unknown, here we consider the sirtuins, a family of NAD+-dependent protein deacetylases that are known to function as regulatory factors that activate or suppress viral transcription and replication in mammals. In particular, we focus on SIRT1 by isolating and characterizing LvSIRT1 from white shrimp (Litopenaeus vannamei) and investigating its involvement in WSSV infection. DsRNA-mediated gene silencing led to the expression of WSSV genes and the replication of genomic DNAs being significantly decreased in LvSIRT1 -silenced shrimp. The deacetylase activity of LvSIRT1 was significantly induced at the early stage (2 hpi) and the genome replication stage (12 hpi) of WSSV replication, but decreased at the late stage of WSSV replication (24 hpi). Treatment with the SIRT1 activator resveratrol further suggested that LvSIRT1 activation increased the expression of several WSSV genes (IE1 , VP28 and ICP11). Lastly, we used transfection and dual luciferase assays in Sf9 insect cells to show that while the overexpression of LvSIRT1 facilitates the promoter activity of WSSV IE1, this enhancement of WSSV IE1 expression is achieved by a transactivation pathway that is NF-κB-independent. • CDNA encoding SIRT1 was identified and characterized from white shrimp (Litopenaeus vannamei). • LvSIRT1 deacetylase activity was induced at the early stage and genome replication stage of WSSV replication. • LvSIRT1 silencing led to the significant decrease in WSSV genes and WSSV genomic DNAs. • LvSIRT1 activation by SIRT1 activator resveratrol increased the expression of several WSSV genes (IE1 , VP28 and ICP11). • Shrimp SIRT1 activates of the WSSV IE1 promoter independently of the NF-κB binding site. [ABSTRACT FROM AUTHOR]