Response of Memory CD8+ T Cells to Severe Acute Respiratory Syndrome (SARS) Coronavirus in Recovered SARS Patients and Healthy Individuals

摘要: To date, the pathogenesis of severe acute respiratory syndrome (SARS) in humans is still not well understood. SARS coronavirus (SARS-CoV)-specific CTL responses, particular their magnitude and duration postinfection immunity, have been extensively studied. In this study, we found that heat-inactivated SARS-CoV elicited recall responses to newly identified spike protein-derived epitopes (SSp-1, S978, S1202) peripheral blood all HLA-A*0201+ recovered patients over 1 year postinfection. Intriguingly, recall-like SSp-1 but S1202, or dominant from several other human viruses 5 36 (13.8%) healthy donors without any contact history with SARS-CoV. SSp-1-specific CTLs expanded memory T cells both patients, five exceptional shared a differentiated effector phenotype, CD45RA+CCR7−CD62L−, expressed CCR5 CD44. However, compared high avidity derived were low avidity, as determined by rapid tetramer dissociation kinetics reduced cytotoxic reactivity, IFN-γ secretion, intracellular production IFN-γ, TNF-α, perforin, granzyme A. These results indicate infection induces strong long-lasting CTL-mediated immunity surviving cross-reactive may exist cell repertoire small subset individuals can be reactivated infection.