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Symptomatic SARS-CoV-2 infections display specific IgG Fc structures (preprint)
medrxiv; 2020.
预印本
在 英语
| medRxiv | ID: ppzbmed-10.1101.2020.05.15.20103341
ABSTRACT
The ongoing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has caused a public health crisis that is exacerbated by our poor understanding of correlates of immunity. SARS-CoV-2 infection can cause Coronavirus Disease 2019 (COVID-19), with a spectrum of symptoms ranging from asymptomatic carriage to life threatening pneumonia and cytokine dysregulation [1-3]. Although antibodies have been shown in a variety of in vitro assays to promote coronavirus infections through mechanisms requiring interactions between IgG antibodies and Fc gamma receptors (Fc{gamma}Rs), the relevance of these observations to coronavirus infections in humans is not known [4-7]. In light of ongoing clinical trials examining convalescent serum therapy for COVID-19 patients and expedited SARS-CoV-2 vaccine testing in humans, it is essential to clarify the role of antibodies in the pathogenesis of COVID-19. Here we show that adults with PCR-diagnosed COVID-19 produce IgG antibodies with a specific Fc domain repertoire that is characterized by reduced fucosylation, a modification that enhances interactions with the activating Fc{gamma}R, Fc{gamma}RIIIa. Fc fucosylation was reduced when compared with SARS-CoV-2-seropositive children and relative to adults with symptomatic influenza virus infections. These results demonstrate an antibody correlate of symptomatic SARS-CoV-2 infections in adults and have implications for novel therapeutic strategies targeting Fc{gamma}RIIIa pathways.
全文:
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采集:
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资料库:
medRxiv
主要主题:
Pneumonia
/
Tumor Virus Infections
/
Coronavirus Infections
/
Severe Acute Respiratory Syndrome
/
COVID-19
语言:
英语
年:
2020
类型:
预印本
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