SARS Immunity and Vaccination

来源 :Cellular & Molecular Immunology | 被引量 : 0次 | 上传用户:gaokao4567
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Severe acute respiratory syndrome (SARS) is a serious and fatal infectious disease caused by SARScoronavirus(SARS-Cov),a novel human coronavirus.SARS-Cov infection stimulates cytokines (e.g.,IL-10,IFN-γ,IL-1,etc.)expression dramatically,and T lymphocytes and their subsets CD4~+ and CD8~+ T cells aredecreased after onset of the disease.SARS-specific IgG antibody is generated in the second week and persistsfor a long time,whereas IgM is expressed transiently.The spike protein and neucleocapsid protein are mostabundant in SARS-Cov and contribute dominantly to the antibody production during the course of disease.Spike protein,especially the ACE-2 binding region(318-510aa)is capable of producing neutralizing antibody toSARS-Cov.Neucleocapsid protein induces protective specific CTL to SARS-Cov.Therefore,applications withspike subunit,neucleocapsid subunit as well as inactivated SARS-Cov are three prospective vaccinationstrategies for SARS.Cellular & Molecular Immunology.2004;1(3):193-198. Severe acute respiratory syndrome (SARS) is a serious and fatal infectious disease caused by SARScoronavirus (SARS-Cov), a novel human coronavirus. SARS-Cov infection stimulates cytokines (eg, IL-10, IFN- γ, IL- 1, etc .) Expression dramatically, and T lymphocytes and their subsets CD4 ~ + and CD8 ~ + T cells are created after onset of the disease. SARS-specific IgG antibodies are generated in the second week and persists for a long time, and IgM is transiently expressed. The spike protein and neucleocapsid protein are mostabundant in SARS-Cov and contribute dominantly to the antibody production during the course of disease. Spike protein, especially the ACE-2 binding region (318-510aa) is capable of producing neutralizing antibody to SARS-Cov. Neucleocapsid protein induces protective specific CTL to SARS-Cov. Beforefore, applications with aspike subunit, neucleocapsid subunit as well as inactivated SARS-Cov are three prospective vaccination strategies for SARS. Cellular & Molecular Immunology. 2004; 1 (3): 193-198.
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