Abstract
Coronavirus disease 2019 (COVID-19), a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes infectious disease, and manifests in a wide range of symptoms from asymptomatic to severe illness and even death. Severity of infection is related to many risk factors, including aging and an array of underlying conditions, such as diabetes, hypertension, chronic obstructive pulmonary disease (COPD), and cancer. It remains poorly understood how these conditions influence the severity of COVID-19. Expansion of the CD28null senescent T-cell populations, a common phenomenon in aging and several chronic inflammatory conditions, is associated with higher morbidity and mortality rates in COVID-19. Here, we summarize the potential mechanisms whereby CD28null cells drive adverse outcomes in disease and predispose patients to devastating COVID-19, and discuss possible treatments for individuals with high counts of CD28null senescent T-cells.
Highlights
SARS-CoV-2 infection (COVID-19) has a broad range of manifestations from asymptomatic carrier states to acute respiratory failure and death
The molecular basis by which aging and the underlying conditions lead to severe COVID-19 remains poorly understood, a growing body of studies demonstrates that hyper-reactive myeloid cells, decreased CD8+ T-cell compartments, and severe lymphopenia contribute to COVID-19 severity [1,2,3,4]
We focus on CD28null T-lymphocytes, another common feature shared by severe COVID-19, aging, and aging-associated chronic conditions, and discuss the potential mechanisms leading to poorer outcomes in COVID-19 and other infectious diseases
Summary
SARS-CoV-2 infection (COVID-19) has a broad range of manifestations from asymptomatic carrier states to acute respiratory failure and death. We focus on CD28null (or CD28− ) T-lymphocytes, another common feature shared by severe COVID-19, aging, and aging-associated chronic conditions, and discuss the potential mechanisms leading to poorer outcomes in COVID-19 and other infectious diseases. Senescence is a natural process of cells irreversibly losing the ability to replicate after a fixed number of replication cycles throughout their life. Because of accumulation of DNA damage and alteration of metabolic and epigenetic programs, these cells largely and express increased levels of surface molecules, OX40, 4-1BB and NK-like receptors. These cells are resistant to apoptosis and steroid treatment and gain a senescence-associated secretory phenotype (SASP).
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