Mechanisms in favor and against COVID-induced carcinogenesis
Against transitory viral infection | In favor of persistent viral infection |
---|---|
Cytopathic effect: SARS-CoV-2 produces extensive tissue damage and cell death that reduces the chances of tumoral transformation. | Immunosuppression: -Lymphopenia and natural killer (NK) cell reduction. -Exhausted NK and CD8+ cells. -Diminished response of interferon. -Induction of pro-tumor cells [myeloid-derived suppressor cell (MDSC), M2 macrophages]. -Decreased CMH-1. -Alterations in autophagy. |
Cell cycle stop. Subsequent apoptosis that impedes tumoral transformation. | Hyperinflammatory and protumoral responses, oxidative stress, cytokine storm: -Severe cases of COVID. -Could induce cellular proliferation, angiogenesis, DNA damage, cytoskeletal remodeling and induction of EMT. |
Direct oncogenic impact. Downregulation of tumor-suppressing proteins [retinoblastoma protein (pRB) and p53]. | |
Reactivation of oncogenic viruses [human papilloma virus (HPV), Epstein-Barr virus (EBV)] |
AO, XMR, JLT, NLM, MLV, SP, and VVB: Conceptualization, Investigation, Writing—original draft, Writing—review & editing. PVN: Conceptualization, Investigation, Methodology, Writing—original draft, Writing—review & editing. AO, XMR, JLT, JZM, and FC: Validation, Writing—review & editing, Supervision. All authors read and approved the submitted version.
The authors declare that they have no conflicts of interest.
Ethical approval is not required in narrative review, according to the institution and relevant policies.
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© The Author(s) 2023.