Low levels of reactive oxygen species (ROS), such as superoxide radical and hydrogen peroxide, are naturally present in insect cell mitochondria due to the incomplete reduction of oxygen in the electron transport chain. However, upon baculoviral infection, insect cells experience increased levels of ROS which causes oxidative stress. This oxidative stress causes protein and lipid damage and contributes to cell death. As the mitochondria are a primary source of ROS production, we have targeted our investigation to this organelle. Prolonged treatment of cells with low concentrations of ethidium bromide has led to the development of two cell lines with non-functional mitochondria. The mitochondrial malfunction has been confirmed by evaluating the cells' respiration parameters and cytochrome-c oxidase activity. Additionally, the cells' doubling time and glucose consumption has been determined. Current experiments are focused on evaluating the oxidative stress and viability of these modified cells during viral infection.