Viral mechanisms contributing to cancer development, with a focus on SARS-CoV-2

MechanismDescriptionImplications for cancerReference
Oncogenic potential of RNA virusesRNA viruses, such as hepatitis C, produce viral proteins that disrupt cellular homeostasis, posing long-term oncogenic risks.Persistent SARS-CoV-2 proteins may drive immune dysregulation, increasing cancer susceptibility.[173, 174]
SARS-CoV-2 specific mechanismsThe spike protein enables viral entry, while nucleocapsid proteins facilitate replication. ACE2 receptor interactions influence tissue susceptibility.SARS-CoV-2 may trigger cellular alterations linked to tumorigenesis, necessitating further investigation.[77, 88, 175]
Chronic inflammationPersistent infections induce prolonged inflammatory responses, promoting a pro-tumorigenic environment.Post-COVID-19 inflammation may enhance cancer risk through sustained immune activation.[100, 176–178]
ImmunosuppressionViral infections compromise immune function, fostering a tumor-permissive microenvironment.Impaired immune surveillance facilitates tumor initiation and progression.[179, 180]
Cellular senescence (CS)Viral infections can induce CS, characterized by growth arrest and a senescence-associated secretory phenotype (SASP).CS may exert dual effects, initially preventing tumors but later promoting chronic inflammation and cancer.[181–183]
DNA modificationViruses can introduce oncogenes, activate proto-oncogenes, or suppress tumor suppressor genes.These genetic disruptions drive oncogenesis, underscoring the need for further molecular studies.[184, 185]
Autophagy dysregulationViral proteins disrupt autophagy, leading to cellular damage accumulation and immune evasion.Impaired autophagy fosters tumor development by promoting cell survival and immune resistance.[186–188]

ACE2: angiotensin-converting enzyme 2; COVID-19: coronavirus disease 2019; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2