SARS-CoV-2 Spike Protein in Intestinal Cells of a Patient with Coronavirus Disease 2019 Multisystem Inflammatory

Juan Mayordomo-Colunga1, Ana Vivanco-Allende2, Inés López-Alonso3

  • 1Department of Pediatrics, Hospital Universitario Central de Asturias, Oviedo, Spain; Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain; Centro de Investigación Biomédica En Red-Enfermedades Respiratorias, Instituto de Salud Carlos III, Madrid, Spain.

The Journal of Pediatrics
|November 29, 2021
PubMed

Insights

A previously healthy child rapidly died from multisystem inflammatory syndrome (MIS-C) linked to SARS-CoV-2. Autopsy revealed a heart clot, and viral spike protein in the gut suggests a possible cause for MIS-C.

Area of Science:

  • Pediatric critical care medicine
  • Infectious diseases
  • Cardiovascular pathology

Background:

  • Multisystem inflammatory syndrome in children (MIS-C) is a rare but serious complication of SARS-CoV-2 infection.
  • The exact pathophysiology of MIS-C remains incompletely understood, posing challenges for timely diagnosis and treatment.
  • Understanding the mechanisms underlying MIS-C is crucial for improving patient outcomes and developing targeted therapies.

Observation:

  • A previously healthy 12-year-old boy presented with severe SARS-CoV-2-related MIS-C.
  • The patient experienced a rapidly fatal clinical course.
  • Autopsy examination identified a significant intracardiac thrombus.

Findings:

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein was identified within intestinal cells.
  • The presence of viral material in the gut supports the hypothesis linking gut viral reservoirs to the systemic immune response in MIS-C.
  • The intracardiac thrombus suggests a potential thrombotic complication contributing to the rapid fatality.

Implications:

  • This case highlights the potential for severe thrombotic events in MIS-C.
  • The findings suggest that the gastrointestinal tract may serve as a reservoir for SARS-CoV-2, triggering or exacerbating the inflammatory cascade in MIS-C.
  • Further research into the gut-immune axis in MIS-C is warranted to explore diagnostic and therapeutic strategies.