More than a year after the start of the pandemic, COVID-19 remains a global health emergency. Although the immune response against SARS-CoV-2 has been extensively studied, some points remain controversial. One is the role of antibodies in viral clearance and modulation of disease severity. While passive transfer of neutralizing antibodies protects against SARS-CoV-2 infection in animal models, titers of anti-SARS-CoV-2 antibodies have been reported to be higher in patients suffering from more severe forms of the disease. A second key question for pandemic management and vaccine design is the persistence of the humoral response. Here, we characterized the antibody response in 187 COVID-19 patients, ranging from asymptomatic individuals to patients who died from COVID-19, and including patients who recovered. We developed in-house ELISAs to measure titers of IgG, IgM and IgA directed against the RBD or N regions in patient serum or plasma, and a spike-pseudotyped neutralization assay to analyse seroneutralization. Higher titers of virus-specific antibodies were detected in patients with severe COVID-19, including deceased patients, compared to asymptomatic patients. This demonstrates that fatal infection is not associated with defective humoral response. Finally, most of recovered patients still had anti-SARS-CoV-2 IgG more than 3Â months after infection.
Development of SARS-CoV2 humoral response including neutralizing antibodies is not sufficient to protect patients against fatal infection.
SARS-CoV-2 体液免疫反应(包括中和抗体)的产生不足以保护患者免受致命感染
阅读:5
作者:Choteau Mathilde, Scohy Anaïs, Messe Stéphane, Luyckx Mathieu, Dechamps Mélanie, Montiel Virginie, Yombi Jean Cyr, Gruson Damien, Limaye Nisha, Michiels Thomas, Dumoutier Laure
| 期刊: | Scientific Reports | 影响因子: | 3.900 |
| 时间: | 2022 | 起止号: | 2022 Feb 8; 12(1):2077 |
| doi: | 10.1038/s41598-022-06038-5 | 研究方向: | 炎症/感染 |
| 疾病类型: | 新冠 | ||
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
