ONCOVIRUSES: how do viruses cause cancer and lead to new therapies?
Objetivo de aprendizagem:To present, in a didactic and up-to-date way, how human oncogenic viruses contribute to cancer development, enabling readers to understand the structure, replication, latency, and oncogenic mechanisms of the main oncoviruses (HPV, HTLV-1, human herpesviruses, polyomaviruses, and hepatitis B, C, and D viruses), as well as to recognize the diagnostic, preventive, and therapeutic strategies associated with these infections
Contexto Educacional:Teaching material developed for the IOC Vacation Course 2026 (Winter Edition) at the Oswaldo Cruz Institute (IOC/Fiocruz). It can also be used for self-study, in undergraduate and graduate courses, and in continuing education and science outreach in health. It focuses on the epidemiological reality and public policies of Brazil (SUS, INCA, Ministry of Health)
Público Alvo:Undergraduate and graduate students in the biological and health sciences (biomedicine, biology, medicine, nursing, pharmacy, among others), health professionals, researchers, and anyone interested in virology, oncology, and public health
Tempo requerido para Aprendizagem:Approximately 30 to 40 hours of study, considering a full reading of the six chapters and review of the concepts. For selective reading, each chapter can be studied independently in about 4 to 6 hours
Oncogenic viruses are associated with a significant proportion of cancer cases worldwide, accounting for approximately 12% of all cancer diagnoses globally. Therefore, they represent an important public health concern. Among the main human oncogenic viruses are human herpesviruses, represented by Epstein-Barr virus (EBV) and human herpesvirus type 8 (HHV-8); human polyomaviruses, including Merkel cell polyomavirus (MCPyV); human papillomaviruses (HPV); human T-cell lymphotropic virus type 1 (HTLV-1); and hepatitis B (HBV), C (HCV), and D (HDV) viruses. In addition to these agents, other viruses, such as herpes simplex virus type 1 (HSV-1), cytomegalovirus (CMV), and BK (BKV) and JC (JCV) polyomaviruses, may act as cofactors, potentiating oncogenic processes associated with other viral infections Viral oncogenesis is a complex and multifactorial process involving different biological mechanisms. Among these, the expression of viral proteins capable of interfering with cellular signaling pathways stands out, promoting the activation of oncogenes, the inactivation of tumor suppressor genes, and the stimulation of uncontrolled cell proliferation. Immune evasion compromises the ability of the immune system to recognize and eliminate infected or transformed cells. Persistent viral infections may also induce chronic inflammation, resulting in increased DNA damage and continuous tissue regeneration, factors that favor the accumulation
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