The role of the histone deacetylase in the replication of Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV) and the immune response of Spodoptera frugiperda cells (Sf9).
Epigenetic mechanisms such as histone changes, especially acetylation and deacetylation, play an important role making host-pathogen interactions by regulating gene expression, which is catalyzed by the enzymes histone acetyltransferase and histone deacetylase. Since one of the safe pest control methods is the use of pathogens, investigating the role of these mechanisms in response to insect pathogens plays a vital role in controlling pests. Studies have shown that histone deacetylase inhibitors affect the replication of mammalian pathogenic viruses. Therefore, in this study, the role of trichostatin as a histone deacetylase inhibitor in Autographacalifornica multicapsid nucleopolyhedrovirus (AcMNPV) virus replication and antiviral immune response in Sf9 cells was investigated. For this purpose, the cells were exposed to two concentrations of trichostatin (1 and 0.25 μM) one and three hours before or at the same time with viral infection and trichostatin effect on virus replication and some important immune system gene expression were investigated. The results showed that virus replication was not affected using this compound. Moreover, after using concentrations of 1 and 0.25 μM trichostatin, the expression level of primary genes of antiviral immune pathways (Ago2 and Dicer2) miRNA and siRNA (Ago1 and Dicer1) did not show significant difference compare with control. In conclusion, the replication of ACMNPV virus and the antiviral immune system in Sf9 cells did not affect by the epigenetic mechanism of histone deacetylation.