There is growing evidence to suggest that severe disease in children infected with common viruses that are typically benign in other children can result from inborn errors of immunity or their phenocopies. Infection with SARS-CoV-2, a cytolytic respiratory RNA virus, can lead to acute hypoxemic COVID-19 pneumonia in children with inborn errors of type I interferon (IFN) immunity or autoantibodies against IFNs. These patients do not appear to be prone to severe disease during infection with EBV, a leukocyte-tropic DNA virus that can establish latency. By contrast, various forms of severe EBV disease, ranging from acute hemophagocytosis to chronic or long-term illnesses, such as agammaglobulinemia and lymphoma, can manifest in children with inborn errors disrupting specific molecular bridges involved in the control of EBV-infected B cells by cytotoxic T cells. The patients with these disorders do not seem to be prone to severe COVID-19 pneumonia. These experiments of nature reveal surprising levels of redundancy of two different arms of immunity, with type I IFN being essential for host defense against SARS-CoV-2 in respiratory epithelial cells, and certain surface molecules on cytotoxic T cells essential for host defense against EBV in B lymphocytes. This article is protected by copyright. All rights reserved.
Keyphrases
- sars cov
- epstein barr virus
- diffuse large b cell lymphoma
- respiratory failure
- young adults
- respiratory syndrome coronavirus
- drug induced
- coronavirus disease
- liver failure
- early onset
- dendritic cells
- emergency department
- genome wide
- immune response
- endothelial cells
- ejection fraction
- patient safety
- magnetic resonance imaging
- dna methylation
- peripheral blood
- computed tomography
- adverse drug
- prognostic factors
- systemic lupus erythematosus
- patient reported outcomes
- acute respiratory distress syndrome
- electronic health record