COVID-19 susceptibility causally related to stroke risk: Using SARS-CoV-2 infection as a natural test of disease predisposition?

Abstract

The COVID-19 pandemic, caused by SARS-CoV-2, has sparked recurring outbreaks and remains endemic, posing ongoing health risks. In addition to its immediate effects, COVID-19 has been linked to cardiovascular complications, including stroke. However, it remains unclear whether COVID-19 causally increases future stroke risk. This study used Mendelian randomization (MR) analysis to explore the causal link between COVID-19 susceptibility and stroke risk. By analyzing genome-wide association study (GWAS) data, genetically determined susceptibility to COVID-19 was identified and linked to various stroke subtypes, including cardioembolic, small-vessel, and large-artery ischemic stroke. Results indicated a significant association between COVID-19 susceptibility and increased stroke risk, particularly for large-artery ischemic stroke. These findings suggest that SARS-CoV-2 infection could serve as a natural indicator of disease predisposition, revealing inherent cardiovascular vulnerabilities. This revolutionizes the way we view pathogen infections—not only as harmful threats, but also as opportunities to assess individual health risks. By analyzing how people respond to infections, we can gain valuable insights into their predisposition to other diseases later in life, offering an analytical framework for early diagnosis and prevention. This perspective—using pathogen infections as natural tests of disease predisposition—offers a transformative way to view human diseases as a continuum. Instead of merely treating infections as isolated diseases, we can exploit natural infections to assess broader population health, thus paving the way for precision medicine and personalized healthcare interventions.