The emergence of SARS-CoV-2, the virus responsible for COVID-19, prompted widespread investigation into its long-term health consequences. A major public health concern revolves around the potential for the infection to initiate or accelerate the development of cancers, particularly aggressive types like brain tumors. Determining any link requires rigorous study due to the complexity of viral biology and the multi-year timeline required for tumor formation. This article examines the current data and biological mechanisms regarding whether COVID-19 can cause a brain tumor, such as gliomas or meningiomas.
The Current Scientific Consensus Regarding Causation
Large-scale epidemiological data do not show a significant increase in the overall incidence of primary brain tumors, such as glioblastoma or meningioma, directly following the COVID-19 pandemic. Brain tumor development typically unfolds over many years, meaning any definitive link between SARS-CoV-2 infection and tumor initiation would likely require a decade or more of follow-up observation. Current studies have primarily focused on the acute and subacute neurological effects, rather than long-term cancer development. Initial analyses of cancer registries revealed that the diagnosis rates for certain non-malignant brain tumors actually decreased during the initial months of the pandemic in 2020. This reduction is attributed to disruptions in medical screening and delayed patient visits.
One specialized genetic study, known as Mendelian randomization, suggested that the genetic predisposition for severe COVID-19 requiring hospitalization might increase the risk of developing glioblastoma. This finding indicates a potential association between the systemic stress of severe infection and later tumor risk. However, it does not constitute direct evidence of the virus causing cancer in the general population, and the lack of an immediate spike in tumor diagnoses across population-level registries remains the strongest counterpoint to a direct causal link.
Biological Plausibility: Viruses and Cancer
The question of whether SARS-CoV-2 could cause a brain tumor is biologically informed by established oncoviruses that can trigger cancer. Viruses are estimated to be responsible for 15% to 20% of all human cancers, including those caused by Human Papillomavirus (HPV), Epstein-Barr Virus (EBV), and Hepatitis B Virus (HBV). These viruses employ distinct mechanisms to transform healthy cells into cancerous ones, often requiring a long latency period spanning 15 to 40 years after the initial infection.
One primary mechanism is genetic integration, where the viral DNA becomes physically incorporated into the host cell’s genome. This integration can disrupt cellular checkpoints or introduce viral proteins, which neutralize tumor suppressor proteins like p53, thereby promoting uncontrolled cell division. Another pathway involves chronic, persistent infection that causes sustained cellular damage and repair cycles. This prolonged state of inflammation leads to oxidative stress and the accumulation of DNA damage, which can eventually result in malignant transformation.
SARS-CoV-2 is an RNA virus, which does not typically integrate into the host genome like DNA oncoviruses, but it can still affect oncogenic pathways. Research indicates that the virus can modulate signaling pathways like NF-κB and MAPK, which regulate cell growth and inflammation. The resulting chronic low-grade inflammation, characteristic of Long COVID, can create an environment permissive to cancer development by suppressing the immune system and promoting tissue damage.
How SARS-CoV-2 Affects the Central Nervous System
While the virus has not been definitively shown to initiate new brain tumors, SARS-CoV-2 affects the central nervous system (CNS) through inflammatory and vascular mechanisms. Neurological symptoms occur in a significant number of patients, ranging from headache and fatigue to cognitive dysfunction, commonly referred to as “brain fog.” These effects are often driven by the body’s immune response rather than massive viral invasion of the brain tissue.
The virus’s presence can trigger neuroinflammation, where inflammatory signaling molecules like cytokines travel from the site of infection through the bloodstream to the brain. This process activates resident immune cells in the brain, called microglia, which can alter communication between neurons and lead to persistent cognitive symptoms. The virus’s ability to cross the blood-brain barrier (BBB) or impair its integrity also contributes to vascular damage, including the formation of microhemorrhages in deeper brain regions.
For patients who already have a brain tumor, the infection may pose a different kind of threat. Studies have observed that SARS-CoV-2 infection may accelerate the progression of existing glioblastoma multiforme (GBM). Tumor hyperprogression was observed shortly after COVID-19 diagnosis in a subset of infected GBM patients, potentially driven by systemic immune disruption and the activation of inflammatory pathways like NF-κB within the tumor microenvironment. These findings highlight the virus’s capacity to influence the tumor environment, even if it does not directly cause the initial cancer.