Adenovirus infection regulates stress granules and P bodies

Objectives: Adenovirus infection promotes the nuclear export of viral late mRNA and inhibits the bulk of cellular mRNA export during the late phase of virus infection. We previously reported that in the late phase of adenovirus infection, AU-rich element (ARE) containing mRNAs are exported to the cytoplasm and are stabilized in order to facilitate adenovirus replication. These results indicate that in the late phase of adenovirus infection, viral late mRNA and ARE-mRNA is exported to the cytoplasm. These results also indicate the regulation system of viral and ARE-mRNA exist in the cytoplasm of adenovirus infected cells. To examine the mechanism of the regulation, we observed a change of stress granule (SG) and P-bodie (PB) during adenovirus infection, because they are thought as cytoplasmic foci which allow some mRNAs to be stored and degraded in them.

Methods: HeLa cells were infected with wild type adenovirus type 5 (wt300), and cells were treated with sodium arsenite and stained them with antibodies for the marker proteins of SG and PB. To detect the adenovirus genes responsible for the change of SG and PB, several mutant viruses were infected and the expression vectors of those genes were introduced into the cells.
Results: In the infected cells, the formation of SG was inhibited even when the cells were treated with arsenite. Furthermore, PB was moved to the peripheral region of the nucleus of the infected cells. From the analysis of the mutant viruses, E1A gene is required for the change of SG and E4orf3 gene is important for the behavior of PB.

Conclusions: Adenovirus controls the behavior of SG and PB to facilitate the expression of viral late mRNA and ARE-mRNA.