Aging in COVID-19: Vulnerability, immunity and intervention

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) pandemic was first reported in Wuhan, China in December 2019, moved across the globe at an unprecedented speed, and is having a profound and yet still unfolding health and socioeconomic impacts. SARS-CoV-2, a beta-coronavirus, is a highly contagious respiratory pathogen that causes a disease that has been termed the 2019 coronavirus disease (COVID-19). Clinical experience thus far indicates that COVID-19 is highly heterogeneous, ranging from being asymptomatic and mild to severe and causing death. Host factors including age, sex, and comorbid conditions are key determinants of disease severity and progression. Aging itself is a prominent risk factor for severe disease and death from COVID19. We hypothesize that age-related decline and dysregulation of immune function, i.e., immunosenescence and inflammaging play a major role in contributing to heightened vulnerability to severe COVID-19 outcomes in older adults. Much remains to be learned about the immune responses to SARS-CoV-2 infection. We need to begin partitioning all immunological outcome data by age to better understand disease heterogeneity and aging. Such knowledge is critical not only for understanding of COVID-19 pathogenesis but also for COVID-19 vaccine development.

Automated summary

The COVID-19 pandemic originating from Wuhan in December 2019 has had far-reaching health and socioeconomic impacts worldwide. The disease caused by SARS-CoV-2 is highly heterogeneous, with age, gender, and comorbidities playing key roles in disease severity and outcomes. Aging and dysregulation of immune function are thought to contribute to the increased vulnerability of older adults to severe COVID-19. Further research on immune responses to SARS-CoV-2 infection, particularly in different age groups, is crucial for understanding disease heterogeneity and developing effective vaccines.