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Background <p>Multisystem inflammatory syndrome in children (MIS-C) is a rare but severe complication that arises between two and six weeks after initial SARS-CoV-2 infection. The mechanisms underlying why only a subset of children develop this hyperinflammatory response remain unclear.</p> Methods <p>We performed an in-depth proteomic analysis of plasma samples from children before and after SARS-CoV-2 infection, including those who developed MIS-C. Proteomic profiling was conducted using high-throughput technologies, and findings were validated using publicly available datasets.</p> Results <p>Healthy children showed minimal changes in the circulating proteome following SARS-CoV-2 infection, with no evidence of ongoing inflammation. In contrast, children with MIS-C exhibited significant activation of pro-inflammatory pathways and elevated circulating markers of myocardial and vascular injury.</p> Conclusions <p>Our data suggest that SARS-CoV-2 infection alone does not cause sustained proteomic alterations in most children. However, MIS-C is associated with a distinct inflammatory and vascular injury signature. Several candidate diagnostic biomarkers for MIS-C were identified and validated in silico, offering promising avenues for future diagnostic and therapeutic strategies.</p>

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In depth characterisation of the proteome of MIS-C and post COVID-19 infection in children reveals inflammatory pathway activation and evidence of tissue damage

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月18日

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  • Cathal Roarty,
  • Claire Tonry,
  • Claire McGinn,
  • Sharon Christie,
  • Tom Waterfield,
  • Chris Watson

摘要

Background

Multisystem inflammatory syndrome in children (MIS-C) is a rare but severe complication that arises between two and six weeks after initial SARS-CoV-2 infection. The mechanisms underlying why only a subset of children develop this hyperinflammatory response remain unclear.

Methods

We performed an in-depth proteomic analysis of plasma samples from children before and after SARS-CoV-2 infection, including those who developed MIS-C. Proteomic profiling was conducted using high-throughput technologies, and findings were validated using publicly available datasets.

Results

Healthy children showed minimal changes in the circulating proteome following SARS-CoV-2 infection, with no evidence of ongoing inflammation. In contrast, children with MIS-C exhibited significant activation of pro-inflammatory pathways and elevated circulating markers of myocardial and vascular injury.

Conclusions

Our data suggest that SARS-CoV-2 infection alone does not cause sustained proteomic alterations in most children. However, MIS-C is associated with a distinct inflammatory and vascular injury signature. Several candidate diagnostic biomarkers for MIS-C were identified and validated in silico, offering promising avenues for future diagnostic and therapeutic strategies.