No retraction, correction or concern found when last checked on Nov 1, 2026.
Superantigenic character of an insert unique to SARS-CoV-2 spike supported by skewed TCR repertoire in patients with hyperinflammation
Mary Hongying Cheng, She Zhang, Rebecca A. Porritt and 6 more
Proceedings of the National Academy of Sciences · 2020 · CC BY
Abstract
Significance A hyperinflammatory syndrome reminiscent of toxic shock syndrome (TSS) is observed in severe COVID-19 patients, including children with Multisystem Inflammatory Syndrome in Children (MIS-C). TSS is typically caused by pathogenic superantigens stimulating excessive activation of the adaptive immune system. We show that SARS-CoV-2 spike contains sequence and structure motifs highly similar to those of a bacterial superantigen and may directly bind T cell receptors. We further report a skewed T cell receptor repertoire in COVID-19 patients with severe hyperinflammation, in support of such a superantigenic effect. Notably, the superantigen-like motif is not present in other SARS family coronaviruses, which may explain the unique potential for SARS-CoV-2 to cause both MIS-C and the cytokine storm observed in adult COVID-19.
Cited by papers we hold 4
- Multisystem inflammatory syndrome in a young adult successfully treated with plasmapheresis, immunoglobulins, and corticosteroids: a case report · 2022Not checked
- SARS-CoV-2-Specific Immune Response and the Pathogenesis of COVID-19 · 2022No notice
- Unraveling the Mystery Surrounding Post-Acute Sequelae of COVID-19 · 2021No notice
- Multisystem Inflammatory Syndrome in Children (MIS-C), a Post-viral Myocarditis and Systemic Vasculitis—A Critical Review of Its Pathogenesis and Treatment · 2020No notice
Reads
Read by people on this page
None yet.
Checked or read by AI through naulon
None yet.
A person counts once a day per paper. We keep no cookie and no address: a reader is a hash that changes every day. Any month under five reads shows no number.
Are you an author?
Is this your paper?
Claim it to add your note and be paid when agents cite it. Free.