Qing-Bin Lu1, Ning Cui2, Jian-Gong Hu3, Wei-Wei Chen4, Wen Xu4, Hao Li3, Xiao-Ai Zhang3, Hinh Ly5, Wei Liu6, Wu-Chun Cao7. 1. School of Public Health, Peking University, Beijing 100191, PR China; State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing 100071, PR China. 2. The 154 Hospital, People's Liberation Army, Xinyang 464000, PR China. 3. State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing 100071, PR China. 4. The 302 Hospital, People's Liberation Army, Beijing 100039, PR China. 5. University of Minnesota, Twin Cities, MN 55108, USA. 6. State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing 100071, PR China. Electronic address: lwbime@163.com. 7. State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing 100071, PR China. Electronic address: caowc@bmi.ac.cn.
Abstract
BACKGROUND: The immunological responses of patients with severe fever with thrombocytopenia syndrome (SFTS) remain largely unknown. We aim to study the magnitude and sustainability of host immune responses and their correlation with clinical, virological and hematological parameters. METHODS: A longitudinal cohort study was performed in a SFTS reference hospital. The sequential immunological evaluation was determined for SFTSV infected patients, including anti-SFTSV IgM, IgG antibodies and the lymphocyte subsets. RESULTS: Altogether 298 laboratory-confirmed SFTS cases were analyzed, from whom 55 patients were followed after convalescence. SFTSV specific IgM antibody could be detected at medium of 9 days, surged to peak levels by 4 weeks, and remained persistent until 6 months after disease onset. SFTSV specific IgG antibody could be detected at medium of 6 weeks; surged to peak levels by 6 months, and remained positive in most of the patients even at 3 years after infection. SFTS patients experienced obvious T cell, B cell and NK cells loss during the first week of infection, which was rapidly restored to normal levels. A significantly lower level of humoral immunity was identified concurrently from severe disease, especially in acute phase of the infection. These abnormalities can be used as a potential indicator in the prediction of an adverse clinical outcome. CONCLUSIONS: Information gained from this study have clinical significance in enhancing our understanding of SFTS immunological characteristics and the disease pathogenesis.
BACKGROUND: The immunological responses of patients with severe fever with thrombocytopenia syndrome (SFTS) remain largely unknown. We aim to study the magnitude and sustainability of host immune responses and their correlation with clinical, virological and hematological parameters. METHODS: A longitudinal cohort study was performed in a SFTS reference hospital. The sequential immunological evaluation was determined for SFTSVinfectedpatients, including anti-SFTSV IgM, IgG antibodies and the lymphocyte subsets. RESULTS: Altogether 298 laboratory-confirmed SFTS cases were analyzed, from whom 55 patients were followed after convalescence. SFTSV specific IgM antibody could be detected at medium of 9 days, surged to peak levels by 4 weeks, and remained persistent until 6 months after disease onset. SFTSV specific IgG antibody could be detected at medium of 6 weeks; surged to peak levels by 6 months, and remained positive in most of the patients even at 3 years after infection. SFTS patients experienced obvious T cell, B cell and NK cells loss during the first week of infection, which was rapidly restored to normal levels. A significantly lower level of humoral immunity was identified concurrently from severe disease, especially in acute phase of the infection. These abnormalities can be used as a potential indicator in the prediction of an adverse clinical outcome. CONCLUSIONS: Information gained from this study have clinical significance in enhancing our understanding of SFTS immunological characteristics and the disease pathogenesis.