Chutima ThepparitKhakpoor, AtefehSarawut KhongwichitNitwara WikanChanida FongsaranPimjai ChingsuwanrotePatcharee PanraksaSmith, Duncan RMahidol University. Institute of Molecular Biosciences. Molecular Pathology LaboratoryMahidol University. Center for Emerging and Neglected Infectious Diseases2015-05-032017-04-252015-05-032017-04-252015-05-032013BMC Research Notes. Vol.6, No.372 (2013), 1-14https://repository.li.mahidol.ac.th/handle/20.500.14594/1815Background A number of studies have implicated the direct involvement of the liver in dengue virus (DENV) infection, and it has been widely shown that liver cells subsequently undergo apoptosis. The mechanism by which liver cells undergo apoptosis in response to DENV infection remains unclear. To provide further information on the mechanism of apoptosis in DENV infected liver cells, HepG2 cells were infected with DENV 2 and analyzed for the induction of ER stress, apoptosis and autophagy. Results In response to DENV infection, HepG2 cells showed the induction of both the ER resident unfolded protein response as well as the Noxa/PUMA stress response pathways. Proteolytic activation of caspases 4, 7, 8 and 9 was observed as well as changes in mitochondrial transmembrane potential. Increased monodansylcadaverine staining was observed in DENV infected cells, consistent with the previously reported induction of autophagy. Conclusions These results are consistent with a model in which the induction of multiple ER stress pathways is coupled with the induction of multiple cell death pathways as a mechanism to ensure the removal of infected liver cells from the system.engMahidol UniversityApoptosisAutophagyCaspaseDengueER stress liverOpen Access articleResearch ArticleBioMed Central10.1186/1756-0500-6-372