The long-term public health implications of COVID-19 extend beyond acute illness, raising concerns about potential chronic diseases. A primary question is whether the SARS-CoV-2 virus acts as a carcinogen, directly increasing the risk of cancer development. This complex inquiry requires distinguishing between the virus’s potential to directly transform cells and the indirect ways the infection’s aftermath might promote a pro-cancer environment in the body. Understanding the true long-term risk depends on separating these two possibilities.
Does SARS-CoV-2 Directly Transform Cells
The mechanism by which a virus directly causes cancer, known as oncogenesis, is typically seen with DNA viruses such as the Human Papillomavirus (HPV) or Epstein-Barr virus (EBV). These DNA viruses integrate their genetic material into the host cell’s genome, activating specific oncogenes that drive uncontrolled cell growth. This process fundamentally transforms a normal cell into a cancer cell.
SARS-CoV-2 is an RNA virus, meaning its genetic material remains primarily in the host cell’s cytoplasm rather than entering the nucleus where the host DNA is housed. This biological difference makes direct genomic integration and subsequent cellular transformation significantly less likely than with DNA viruses. While some RNA viruses, like Hepatitis C (HCV), are linked to cancer, they usually act indirectly by causing chronic inflammation and organ damage over decades.
Researchers have explored whether SARS-CoV-2 proteins interfere with cell cycle regulation, a hallmark of cancer development. Studies suggest that certain viral proteins, such as non-structural protein 3 (Nsp3), might interact with and promote the degradation of tumor suppressor proteins like p53. Since p53 normally triggers cell death or repair when DNA damage occurs, its degradation could disrupt the body’s natural defense against malignancy.
Other viral proteins, including ORF6 and Nsp13, have been shown in laboratory settings to potentially cause DNA damage and impair the host’s repair mechanisms. These findings suggest that while SARS-CoV-2 is not a classical oncogenic virus, its components may create a state of genomic instability within infected cells. The virus lacks the inherent machinery for direct, long-term cellular transformation but may still disrupt pathways that prevent cancer.
How Inflammation Creates a Pro-Cancer Environment
The most plausible link between COVID-19 and increased cancer risk is through chronic, systemic inflammation. Acute SARS-CoV-2 infection can trigger an intense immune response, sometimes resulting in a “cytokine storm,” where the body releases high levels of pro-inflammatory signaling molecules. Even after the initial infection clears, many individuals, particularly those with Long COVID, experience persistent, low-grade inflammation, which is a known driver of carcinogenesis.
This prolonged inflammatory state leads to the continuous production of reactive oxygen species (ROS) and other cellular byproducts that can directly cause DNA damage. When this damage accumulates without adequate repair, it increases the likelihood of mutations that lead to uncontrolled cell proliferation. Chronic inflammatory signaling also creates a microenvironment conducive to tumor growth and progression.
Severe infection can also induce cellular senescence, often described as stress-induced aging. Senescent cells stop dividing but remain metabolically active, secreting a mix of inflammatory molecules called the Senescence-Associated Secretory Phenotype (SASP). These SASP factors, including interleukins and chemokines, sustain chronic inflammation and actively promote the growth of nearby pre-malignant cells.
Finally, the infection affects the immune system’s ability to police the body for nascent cancer cells, a process called immune surveillance. Severe COVID-19 can lead to T-cell exhaustion and general immune dysregulation, characterized by a reduction in protective white blood cells. When immune defenses are compromised, the body struggles to detect and eliminate abnormal cells before they establish themselves as tumors.
What Population Studies Show About New Diagnoses
Analyzing large-scale population studies provides real-world data, though the results are complicated by the pandemic’s impact on healthcare access. During the initial waves, many countries reported a sharp decrease in new cancer diagnoses because screening programs and routine doctor visits were postponed or canceled. This decline suggested a significant backlog of undetected cases.
Recent studies tracking cancer incidence over time have provided more nuanced data. For example, one large cohort study in Southern Italy found that the incidence of new cancer diagnoses rose significantly during the pandemic compared to pre-pandemic years. This increase was observed across various age groups and included a rise in diagnoses of specific cancers, such as brain and skin cancers.
In contrast, data from the U.S. Surveillance, Epidemiology, and End Results (SEER) program showed that overall cancer incidence rates in 2021 remained lower than expected based on pre-pandemic trends. This finding suggests that a deficit of undiagnosed cases persisted through the second year of the pandemic, amounting to tens of thousands of missed diagnoses. The lack of a significant “rebound” in diagnoses is concerning.
The long-term epidemiological challenge is the necessary latency period for cancer development, which spans several years or decades. Current population data largely reflect short-term trends heavily influenced by screening disruptions and delayed care. Therefore, the full scope of a post-COVID cancer risk—whether due to the virus itself or the delayed diagnosis of more advanced disease—will require monitoring over the next several years.
Effects on Individuals Already Living with Cancer
For individuals already diagnosed with cancer, the impact of a subsequent COVID-19 infection is distinct from the question of cancer causation. Cancer patients are considered immunocompromised, either due to the malignancy itself or the treatments they receive, placing them at a higher risk for severe illness from SARS-CoV-2. Studies consistently show that these patients, particularly those with hematological (blood) cancers or metastatic disease, have a higher risk of severe complications and mortality if they contract COVID-19.
The pandemic response also affected the continuity of cancer care delivery. Many patients experienced delays in receiving treatments such as chemotherapy, radiation, or surgery due to hospital capacity issues and resource redirection. These treatment delays can negatively impact prognosis and increase the risk of the cancer progressing or recurring.
In addition to the immediate threat of severe infection, the inflammatory response triggered by COVID-19 could theoretically accelerate the progression of existing tumors. Conversely, some rare case reports have documented temporary tumor shrinkage following infection, suggesting robust immune activation can sometimes have an anti-tumor effect. Overall, the evidence points to an increased risk of severe outcomes and complications in the management of cancer for those who contract the virus.