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)] |