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Response of Memory CD8⁺ T Cells to Severe Acute Respiratory Syndrome (SARS) Coronavirus in Recovered SARS Patients and Healthy Individuals¹

Huabiao Chen^*, Jinlin Hou, Xiaodong Jiang, Shiwu Ma, Minjie Meng, Baomei Wang^*, Minghui Zhang^*, Mingxia Zhang, Xiaoping Tang^¶, Fuchun Zhang^¶, Tao Wan^*, Nan Li^*, Yizhi Yu^*, Hongbo Hu^||, Ruifu Yang^#, Wei He^||, Xiaoning Wang and Xuetao Cao^2,*,

^* Institute of Immunology, Second Military Medical University, Shanghai, China; Department of Infectious Diseases, Nanfang Hospital, First Military Medical University, Guangzhou, China; Institute of Immunology, Zhejiang University, Hangzhou, China; Institute of Molecular Immunology, First Military Medical University, Guangzhou, China; ^¶ Institute of Infectious Diseases, No. 8 People’s Hospital, Guangzhou, China; ^|| Department of Immunology, Institute of Basic Medical Sciences, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, China; and ^# Institute of Microbiology and Epidemiology, Chinese Academy of Military Medical Sciences, Beijing, China

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

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