Mechanisms in favor and against COVID-induced carcinogenesis

Against transitory viral infectionIn 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)]