Exploring the oncogenic potential of SARS-CoV-2 in the gastrointestinal tract

Table 1 Key mechanisms of severe acute respiratory syndrome coronavirus 2 in gastrointestinal oncogenesis

Key mechanisms	Description	Potential implications
SARS-CoV-2 viral entry and replication in GI tract	SARS-CoV-2 utilizes ACE2 receptors for cellular entry in the GI tract, triggering intracellular responses	Alteration of GI homeostasis, increased viral persistence, and systemic inflammation
Chronic inflammation and immune dysregulation	Persistent inflammation can lead to genetic instability, cell transformation, and increased cancer risk	Long-term tissue damage, enhanced susceptibility to malignancies
Potential viral integration into host DNA	Hypothetical integration of viral RNA into host DNA may cause genetic mutations and epigenetic alterations	Potential genomic instability, requiring further investigation
Gut microbiome dysbiosis and GI malignancy risk	Gut microbiota disruption linked to colorectal cancer progression due to immune suppression and chronic inflammation	Possible link between COVID-19 recovery and long-term cancer risk
Immune escape and oncogenesis	Mutations enabling immune escape may promote persistent viral presence and tumorigenesis	Emergence of new variants with oncogenic potential

SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2; ACE2: Angiotensin-converting enzyme 2; GI: Gastrointestinal; COVID-19: Coronavirus disease 2019.