Epidemiology of Exposures, Preceding Illness and Testing History in Children With Multisystem Inflammatory Syndrome in Children in the First 18 Months of the COVID-19 Pandemic, Los Angeles County, California

Newhouse, Caitlin N; Finn, Lauren E.; Gragnani, Candace M; Hathaway, Susan; Nunez, Denise M.; Malenfant, Jason H; Fernandes, Priyanka; Kim, Moon J.; Terashita, Dawn; Balter, Sharon

doi:10.1097/inf.0000000000003688

Cited by 1 publication

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“…T cell receptor sequencing has been performed on all these groups, including Kawasaki disease (KD) (see sources referenced in the Section 4 ) providing the possibility of exploring whether these TCR sequences unexpectedly mimic SARS-CoV-2. Since the cause or causes of KD are unknown and range from viruses to bacteria to vaccines [ 53 , 54 , 55 , 56 , 57 ], and since KD was discovered long before SARS-CoV-2 was identified, KD TCRs provide good control for MIS-C TCRs.…”

Section: Introductionmentioning

confidence: 99%

T Cell Receptor Sequences Amplified during Severe COVID-19 and Multisystem Inflammatory Syndrome in Children Mimic SARS-CoV-2, Its Bacterial Co-Infections and Host Autoantigens

Root‐Bernstein

Churchill

Oliverio

2023

IJMS

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Published hypervariable region V-beta T cell receptor (TCR) sequences were collected from people with severe COVID-19 characterized by having various autoimmune complications, including blood coagulopathies and cardiac autoimmunity, as well as from patients diagnosed with the Kawasaki disease (KD)-like multisystem inflammatory syndrome in children (MIS-C). These were compared with comparable published v-beta TCR sequences from people diagnosed with KD and from healthy individuals. Since TCR V-beta sequences are supposed to be complementary to antigens that induce clonal expansion, it was surprising that only a quarter of the TCR sequences derived from severe COVID-19 and MIS-C patients mimicked SARS-CoV-2 proteins. Thirty percent of the KD-derived TCR mimicked coronaviruses other than SARS-CoV-2. In contrast, only three percent of the TCR sequences from healthy individuals and those diagnosed with autoimmune myocarditis displayed similarities to any coronavirus. In each disease, significant increases were found in the amount of TCRs from healthy individuals mimicking specific bacterial co-infections (especially Enterococcus faecium, Staphylococcal and Streptococcal antigens) and host autoantigens targeted by autoimmune diseases (especially myosin, collagen, phospholipid-associated proteins, and blood coagulation proteins). Theoretical explanations for these surprising observations and implications to unravel the causes of autoimmune diseases are explored.

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