SARS-CoV-2 Interactions with Cancer Biology

Since the emergence of SARS-CoV-2, numerous studies have explored its influence on cancer biology. The virus can modulate host immunity, tumour metabolism and the tumour microenvironment in ways that may both hinder and promote malignancy. Severe infection often triggers a hyperinflammatory cytokine storm, which can damage tissues and impair antitumour immunity, yet paradoxically this response has, in rare cases, coincided with spontaneous tumour regression. At a molecular level, SARS-CoV-2 proteins interact with autophagy and metabolic pathways, alter oncosuppressor function and drive chronic low-grade inflammation that may predispose survivors to oncogenesis, particularly in the context of long COVID. Conversely, oncolytic effects have been proposed, whereby viral antigens provoke cross-reactive immune responses, reactivating cytotoxic lymphocytes against neoplastic cells. Beyond immunological mechanisms, emerging data suggest reverse transcription of viral RNA, potential genomic integration and epigenetic dysregulation, raising questions about long-term genomic stability and cancer risk. Understanding these multifaceted interactions is essential for optimising cancer management during and after COVID-19 and may inform innovative therapeutic strategies that exploit virus-induced immune reawakening.

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SARS-CoV-2 Interactions with Cancer Biology publication trend

The graph below shows the total number of articles in sars-cov-2 interactions with cancer biology across all publications each year (not limited to Nature Index journals).

Technical terms

Cytokine storm: A dysregulated, hyperinflammatory response characterised by excessive release of cytokines that can lead to tissue damage and organ dysfunction.

Oncolytic virus: A virus that selectively infects and lyses cancer cells, often provoking secondary antitumour immune responses.

Autophagy: A cellular process for degrading and recycling cytoplasmic components via lysosomal pathways, which influences cell survival and death.

Oncogenic pathway: A sequence of molecular events and signalling cascades that drive the initiation, growth and survival of cancer cells.

Tumour microenvironment: The complex milieu of stromal cells, immune cells, extracellular matrix and signalling molecules surrounding and interacting with tumour cells.

Tumour suppressor: A gene or protein that inhibits cell proliferation, promotes apoptosis or maintains genomic integrity to prevent tumour formation.

References

1. Spontaneous cancer remission after COVID-19: insights from the pandemic and their relevance for cancer treatment. Journal of Translational Medicine (2023).
2. Deciphering the Relationship between SARS-CoV-2 and Cancer. International Journal of Molecular Sciences (2023).
3. Should We Expect an Increase in the Number of Cancer Cases in People with Long COVID?. Microorganisms (2023).
4. Reverse-transcribed SARS-CoV-2 RNA can integrate into the genome of cultured human cells and can be expressed in patient-derived tissues. Proceedings of the National Academy of Sciences of the United States of America (2021).
5. Exogenous Coronavirus Interacts With Endogenous Retrotransposon in Human Cells. Frontiers in Cellular and Infection Microbiology (2021).
6. SARS-CoV-2 as an Oncolytic Virus Following Reactivation of the Immune System: A Review. International Journal of Molecular Sciences (2023).
7. Potential Molecular Mechanisms of Rare Anti-Tumor Immune Response by SARS-CoV-2 in Isolated Cases of Lymphomas. Viruses (2021).