It has been demonstrated that damage caused by oxidative stress contributes to the death of baculovirus infected insect cells. We hypothesize that the oxidative stress primarily results from increased synthesis of reactive oxygen species in the mitochondria. One approach to testing this hypothesis is to investigate the effect of baculovirus infection on host insect cells that lack mitochondria. Two types of insect cells were studied: Spodoptera frugiperda (Sf-9) and Trichoplusia ni (Tn-5). The cells were grown in media with low amounts of ethidium bromide, which selectively mutates mitochondrial DNA to remove functional mitochondria. Consistent with our hypothesis, baculovirus infection of these EtBr-treated cells is inhibited and the oxidative stress in these cells is significantly reduced compared to cells with functional mitochondria. Work involved with obtaining the mitochondria free cells and the application of the resulting cells will be discussed.