The question of whether COVID-19 infection can cause breast cancer is a source of significant public concern, fueled by the virus’s widespread impact and the complexity of cancer biology. While the virus, SARS-CoV-2, does not follow the pattern of established cancer-causing viruses, scientists are actively investigating how the profound physiological changes it induces might influence cancer development or progression. Understanding the link requires separating the theoretical biological mechanisms from the concrete data observed in large populations. Current evidence suggests that any connection is indirect, tied more to the body’s inflammatory response and the disruption of healthcare systems than to the virus directly initiating a tumor.
Evaluating Direct Carcinogenesis
The initial step in assessing a viral link to cancer is determining if the virus is an oncogenic agent. Unlike viruses such as Human Papillomavirus (HPV) or Hepatitis B (HBV), SARS-CoV-2 is not classified as a classic oncovirus that integrates its genetic material into the host cell’s DNA to initiate a tumor. Classic oncoviruses typically introduce oncogenes or permanently disrupt tumor-suppressor genes, forcing the cell toward malignant transformation.
However, research has identified indirect mechanisms by which the virus’s components could theoretically promote an existing precancerous state. Viral proteins, such as non-structural proteins (Nsp3, Nsp15) and the S2 subunit, have been shown in laboratory settings to interact with key tumor-suppressor proteins. Specifically, these viral elements may interfere with the function of p53 and the retinoblastoma protein (Rb), which regulate cell division and initiate programmed cell death. By temporarily dampening these surveillance systems, the virus may create an environment conducive to the survival and proliferation of already damaged cells.
Systemic Inflammation and Cancer Risk
The most recognized theoretical link between COVID-19 and cancer risk centers on the body’s intense inflammatory response to the infection. Severe COVID-19 often triggers a “cytokine storm,” a massive, uncontrolled release of pro-inflammatory signaling molecules like Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α). Chronic inflammation is a well-established risk factor for many cancers, as these signaling molecules can promote cellular proliferation, new blood vessel formation (angiogenesis), and resistance to cell death.
This inflammatory state can also severely impair the immune system’s ability to detect and destroy nascent cancer cells, a process called immune surveillance. Severe SARS-CoV-2 infection is often characterized by lymphopenia, a reduction in critical immune cells, including CD4+ and CD8+ T-cells. This T-cell dysregulation, sometimes described as T-cell exhaustion, compromises the immune system’s capacity to eliminate cancerous cells before they can establish a tumor.
Furthermore, a persistent, low-grade inflammatory state, which is a feature of some cases of Long COVID, could sustain a pro-tumor microenvironment long after the acute infection resolves. The continuous presence of inflammatory factors and oxidative stress contributes to DNA damage and genetic instability. This potentially accelerates the growth of dormant or microscopic breast tumors, meaning the virus acts as a potent promoter of progression rather than an initiator of cancer.
Current Epidemiological Findings
Despite these plausible biological theories, large-scale population studies and cancer registry data currently do not support a surge in the overall incidence of new breast cancer diagnoses directly attributable to SARS-CoV-2 infection. In fact, most epidemiological data from the peak pandemic years of 2020 and 2021 showed a significant decrease in the number of new breast cancer cases identified. Screening mammography rates dropped dramatically, in some regions by over 40%, and the overall number of breast cancer diagnoses fell by an estimated 18% to 29%.
This apparent decrease is not a sign that the infection is protective; rather, it reflects a large backlog of undiagnosed cases due to missed screenings. When cancers were diagnosed during this period, they were more likely to be found at a later stage, such as Stage II or higher, or when the patient presented with noticeable symptoms. This shift toward later-stage diagnoses is a direct consequence of the disruption to preventative care, which is designed to catch tumors when they are small and asymptomatic.
While long-term studies are ongoing to track cancer rates in individuals who had severe COVID-19, the current consensus from major health organizations is that the immediate threat to public health is the delay in diagnosis, not an elevated cancer risk from the virus itself. The limited follow-up time since the start of the pandemic means that any potential long-term, virus-driven increase in cancer incidence, which can take years to manifest, may not yet be evident in the data.
Impact on Screening and Detection
The most immediate and demonstrable impact of the pandemic on breast cancer has been on the logistics of detection, creating two distinct diagnostic challenges. The first was the widespread interruption of routine screening programs, which led to a substantial reduction in the diagnosis of early-stage breast cancer. Studies have shown that many women were diagnosed with more advanced disease because their scheduled mammograms were postponed or canceled during lockdowns.
The second challenge involves a specific diagnostic artifact caused by the immune response to the virus or the vaccine. Both a natural COVID-19 infection and, more frequently, the COVID-19 vaccines can cause axillary lymphadenopathy, or swelling of the lymph nodes in the armpit region. This swelling is a normal sign of an immune response, but enlarged lymph nodes are also a common sign of breast cancer metastasis on a mammogram.
This phenomenon created diagnostic confusion, temporarily leading to “false positive” or indeterminate results on imaging that required follow-up. The enlarged nodes can persist for weeks or even months, prompting health guidelines to recommend scheduling screening mammograms four to six weeks after vaccination. This ensures the nodes have returned to normal size, preventing unnecessary biopsies or additional imaging.