The long-term health consequences of SARS-CoV-2 infection remain a focus of scientific inquiry. A pressing question is whether contracting the virus increases a person’s risk of developing cancer. The relationship is complex, involving direct biological effects from the virus and indirect systemic risks related to the infection’s aftermath and disruptions to healthcare systems. Analyzing the current scientific consensus requires distinguishing between the virus’s potential to initiate new tumors and its ability to accelerate the progression of existing or pre-cancerous conditions.
Direct Viral Impact on Tumor Initiation
The primary question is whether SARS-CoV-2 acts as an oncogenic virus, meaning one that directly causes new tumors. Oncogenic viruses, like Human Papillomavirus (HPV), integrate genetic material or produce proteins that interfere with cellular growth control. Currently, there is no strong epidemiological evidence suggesting that COVID-19 infection directly initiates new tumors.
SARS-CoV-2 is an RNA virus. Cancer causation by RNA viruses often involves chronic infection or the integration of a reverse-transcribed DNA copy into the host cell’s genome. While some studies suggested SARS-CoV-2 RNA could be reverse-transcribed, advanced sequencing techniques have failed to find evidence of such integration in vivo. Thus, SARS-CoV-2 does not possess the characteristics of a classical cancer-causing virus.
The virus enters cells via the Angiotensin-Converting Enzyme 2 (ACE2) receptor, expressed in many tissues. However, the transient nature of most acute infections argues against the long-term changes necessary for cancer initiation. Initiation typically requires sustained interference with tumor-suppressor genes or chronic cell damage. Therefore, the risk of COVID-19 acting as a direct initiator of cancer is currently considered low.
Biological Pathways Affecting Cancer Progression
While direct initiation is unlikely, a more significant concern lies in indirect biological mechanisms that could accelerate the progression of existing cancer or pre-cancerous lesions. The link involves the environment created by the body’s response to the infection, particularly chronic systemic inflammation and immune system dysregulation.
Acute SARS-CoV-2 infection can trigger a massive release of pro-inflammatory signaling molecules, known as a cytokine storm. Many survivors, particularly those with “long COVID,” experience persistent, low-grade inflammation even after the acute phase resolves. This chronic inflammatory environment is a well-established risk factor for cancer, promoting cellular proliferation, DNA damage, and favoring the growth of malignant cells.
The infection can also profoundly affect immunosurveillance—the immune system’s ability to destroy nascent cancer cells. The immune response to the virus can lead to the exhaustion of T-cells, which are crucial for eliminating cancer cells. This impairment of T-cell and Natural Killer (NK) cell function could allow microscopic or dormant tumors to evade detection and grow. Studies show that inflammation triggered by COVID-19 can awaken dormant disseminated cancer cells (DCCs) in the lungs, increasing the risk of metastatic progression.
Delayed Screening and Treatment Risks
Beyond the biological effects of the virus, the pandemic created a substantial risk to cancer outcomes due to severe disruptions in healthcare services. Public health measures, hospital capacity constraints, and patient hesitancy led to a dramatic decrease in routine cancer screening and diagnostic procedures worldwide.
During the peak periods, screening rates for common cancers plummeted; for instance, screenings for breast, colorectal, and lung cancers saw reductions ranging from 56% to 85% in the U.S. in early 2020. This avoidance of routine care resulted in an estimated 22 million missed cancer screenings, contributing to a significant decline in newly diagnosed cancer cases.
The consequence of these missed appointments is an increase in late-stage cancer diagnoses, as tumors had more time to progress undetected. Delays in diagnosis result in the cancer being more advanced, limiting treatment options and worsening the prognosis. Additionally, active cancer treatment regimens were often interrupted or modified to reduce the risk of severe COVID-19 infection in vulnerable patients, further impacting survival rates.
Summary of Current Scientific Findings
The current scientific evidence distinguishes between the viral agent and the environment. There is little evidence that SARS-CoV-2 acts as a classical oncogenic virus that directly initiates tumors in the general population.
The stronger and more immediate risk stems from indirect effects, primarily the creation of a pro-tumorigenic environment following infection. Chronic inflammation and immune dysregulation post-COVID are plausible mechanisms that could accelerate the growth of existing tumors or awaken dormant cancer cells, particularly in the lungs. Observational data supports this, showing that cancer survivors who contracted the virus had an increased risk of dying from metastatic cancer.
Furthermore, the systemic disruption to cancer care caused by the pandemic—resulting in delayed screenings and diagnoses—represents a tangible risk factor that has already led to an increase in late-stage cancers. To fully understand the long-term impact, multi-year longitudinal studies are required to track cancer incidence in COVID-19 survivors.