Introduction: The role of oxidative stress in the pathogenesis of neoplastic diseases, including its connection with viral infections, is the subject of many publications. The results of numerous researches have revealed that virus-induced phagocyte activation is associated with oxidative stress, not only because reactive oxygen species (ROS) are released, but also because activated phagocytes can release cytokines, such as tumour necrosis factor (TNF-alpha) or interleukin-1 (IL-1). Objective: The purpose of this review is to analyze the role of ROS in the pathogenesis of head and neck cancer and correlation between ROS and viruses, especially Epstein-Barr virus (EBV) and Human papillomavirus (HPV), in malignant tumour development in this area. State of knowledge: The effects of an increased amount of ROS or reactive nitrate species (RNS) with a simultaneous reduction of antioxidants are noticed in various cancers, including head and neck cancer. Increased oxidative stress is also associated with disorders in the antioxidant defence system. HPV and EBV, which are important risk factors for head and neck cancer, can act via ROS-based mechanisms. Long-term expression of the Epstein–Barr nuclear antigen 1 (EBNA1) causes increased ROS and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase level. During expression of HPV16- infected cells, RNS increase E6 and E7 levels, thereby increasing the level of DNA damage in the cell. ROS are also involved in many benign oral disorders. Conclusions: Reactive oxygen species are involved in various pathological processes in the environment of chronic oxidative stress, including carcinogenicity. ROS contribute to the development of head and neck cancer through many risk factors, such as connection with viruses.