期刊
ACS INFECTIOUS DISEASES
卷 2, 期 5, 页码 361-376出版社
AMER CHEMICAL SOC
DOI: 10.1021/acsinfecdis.6b00006
关键词
SARS-CoV; peptide; vaccine; antibody-dependent enhancement (ADE); epitope sequence-dependent (ESD) enhancement; B-cell peptide epitope
资金
- National Institute of Allergy and Infectious Diseases [U01AI061092]
- National Natural Science Foundation of China [90713045]
- Fundamental Studies in Health Sciences of the NIBIO [04-2]
Severe acute respiratory syndrome (SARS) is caused by a coronavirus (SARS-CoV) and has the potential to threaten global public health and socioeconomic stability. Evidence of antibody-dependent enhancement (AIDE) of SARS-CoV infection in vitro and in non-human primates clouds the prospects for a safe vaccine. Using antibodies from SARS patients, we identified and characterized SARS-CoV B-cell peptide epitopes with disparate functions. In rhesus macaques, the spike glycoprotein peptides S471-503, S604-625, and S1164-1191 elicited antibodies that efficiently prevented infection in non-human primates. In contrast, peptide S597-603 induced antibodies that enhanced infection both in vitro and in non-human primates by using an epitope sequence-dependent (ESD) mechanism. This peptide exhibited a high level of serological reactivity (64%), which resulted from the additive responses of two tandem epitopes (S597-603 and S604-625) and a long-term human B-cell memory response with antisera from convalescent SARS patients. Thus, peptide-based vaccines against SARS-CoV could be engineered to avoid ADE via elimination of the S597-603 epitope. We provide herein an alternative strategy to prepare a safe and effective vaccine for ADE of viral infection by identifying and eliminating epitope sequence-dependent enhancement of viral infection.
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