# Biomarkers of long COVID in children and young adults: a scoping review

**Authors:** Bettina Camara, Danilo Buonsenso

PMC · DOI: 10.1007/s00431-026-06789-7 · 2026-02-16

## TL;DR

This review identifies biomarkers in children and young adults with long COVID, suggesting physiological causes for their symptoms.

## Contribution

The study compiles 41 biomarker occurrences in pediatric long COVID patients, linking them to physiological symptoms.

## Key findings

- 41 biomarker occurrences were identified across nine studies, showing significant differences from healthy controls.
- Biomarkers suggest physiological manifestations of long COVID in pediatric populations.
- More research is needed to clarify risk factors and immune pathways in young patients.

## Abstract

Following the SARS-CoV-2 pandemic, a significant percentage of people are now experiencing long-term symptoms, despite a continuing lack of concrete documentation of physiological and risk profiles that hinders diagnosis and treatment, particularly in pediatric contexts. This review aims to highlight the existing evidence for measurable physiological markers for post-acute sequelae of SARS-CoV-2 infection (long COVID) in children, adolescents, and young adults. Titles providing data related to measurable biomarkers distinguishing young long COVID patients from controls were compiled and analyzed. Results were displayed in table and diagram form for optimal qualitative evaluation of the relationship between markers and symptomatology within the context of each organ system. Only human studies published in English, Italian, Portuguese, German, and Spanish between the 5th of February 2025 and the 31st of December 2025 were considered, and no other time constraints were applied. Following search and criteria evaluation, nine studies were included, totaling 41 occurrences identified in diseased patients with statistically significant variation from healthy controls. Markers suggest the presence of organic manifestations based on published literature, although more data and future studies will be necessary to establish clear connections.

Conclusion: The data compiled for this review adds to the body of evidence indicating a physiological manifestation of long COVID and its consequences. Further investigation into potential risk factors, pre- and post-pubescent manifestations, and specific inflammatory and immune pathways will be necessary for a more concrete understanding of long COVID and its effects on children, adolescents, and young adults.

What is Known:• Long COVID is estimated to affect a significant population of patients, despite the lack of concrete physiological diagnostic and prognostic measures.• Pediatric incidence of the disease is still largely debated, and published data are scarce.What is New:• A total of 41 biomarker occurrences were identified by selected studies, which were consistent with expected physiology behind reported symptoms.• The body of data discussed suggests the presence of physiological phenomena behind the long-term symptoms experienced by pediatric long- COVID patients.

What is Known:

• Long COVID is estimated to affect a significant population of patients, despite the lack of concrete physiological diagnostic and prognostic measures.

• Pediatric incidence of the disease is still largely debated, and published data are scarce.

What is New:

• A total of 41 biomarker occurrences were identified by selected studies, which were consistent with expected physiology behind reported symptoms.

• The body of data discussed suggests the presence of physiological phenomena behind the long-term symptoms experienced by pediatric long- COVID patients.

The online version contains supplementary material available at 10.1007/s00431-026-06789-7.

## Full-text entities

- **Genes:** CXCL10 (C-X-C motif chemokine ligand 10) [NCBI Gene 3627] {aka C7, IFI10, INP10, IP-10, SCYB10, crg-2}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, TNFSF11 (TNF superfamily member 11) [NCBI Gene 8600] {aka CD254, ODF, OPGL, OPTB2, RANKL, TNLG6B}, CXCL11 (C-X-C motif chemokine ligand 11) [NCBI Gene 6373] {aka H174, I-TAC, IP-9, IP9, SCYB11, SCYB9B}, CD40 (CD40 molecule) [NCBI Gene 958] {aka Bp50, CDW40, TNFRSF5, p50}, CCL23 (C-C motif chemokine ligand 23) [NCBI Gene 6368] {aka CK-BETA-8, CKb8, Ckb-8, Ckb-8-1, MIP-3, MIP3}, SELP (selectin P) [NCBI Gene 6403] {aka CD62, CD62P, GMP140, GRMP, LECAM3, PADGEM}, CXCL5 (C-X-C motif chemokine ligand 5) [NCBI Gene 6374] {aka ENA-78, SCYB5}, IL2 (interleukin 2) [NCBI Gene 3558] {aka IL-2, TCGF, lymphokine}, CXCL6 (C-X-C motif chemokine ligand 6) [NCBI Gene 6372] {aka CKA-3, GCP-2, GCP2, SCYB6}, CD5 (CD5 molecule) [NCBI Gene 921] {aka LEU1, T1}, FLT3LG (fms related receptor tyrosine kinase 3 ligand) [NCBI Gene 2323] {aka FL, FLG3L, FLT3L, IMD125}, IL21 (interleukin 21) [NCBI Gene 59067] {aka CVID11, IL-21, Za11}, ADA (adenosine deaminase) [NCBI Gene 100] {aka ADA1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CXCL1 (C-X-C motif chemokine ligand 1) [NCBI Gene 2919] {aka FSP, GRO1, GROa, MGSA, MGSA-a, NAP-3}, ADA2 (adenosine deaminase 2) [NCBI Gene 51816] {aka ADGF, CECR1, IDGFL, PAN, SNEDS, VAIHS}, CRYGD (crystallin gamma D) [NCBI Gene 1421] {aka CACA, CCA3, CCP, CRYG4, CTRCT4, PCC}, TADA1 (transcriptional adaptor 1) [NCBI Gene 117143] {aka ADA1, HFI1, STAF42, TADA1L, hADA1}, CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347] {aka GDCF-2, HC11, HSMCR30, MCAF, MCP-1, MCP1}, OSM (oncostatin M) [NCBI Gene 5008], IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, VWF (von Willebrand factor) [NCBI Gene 7450] {aka F8VWF, VWD}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, PLAU (plasminogen activator, urokinase) [NCBI Gene 5328] {aka ATF, BDPLT5, QPD, UPA, URK, u-PA}, TGFA (transforming growth factor alpha) [NCBI Gene 7039] {aka TFGA}, CCL3 (C-C motif chemokine ligand 3) [NCBI Gene 6348] {aka G0S19-1, LD78, LD78ALPHA, MIP-1-alpha, MIP1A, SCI}, IL18R1 (interleukin 18 receptor 1) [NCBI Gene 8809] {aka CD218a, CDw218a, IL-18R, IL-18R-alpha, IL-18Ralpha, IL-1Rrp}, ACE2 (angiotensin converting enzyme 2) [NCBI Gene 59272] {aka ACEH}, CCL11 (C-C motif chemokine ligand 11) [NCBI Gene 6356] {aka SCYA11}
- **Diseases:** POTS (MESH:D054972), thrombotic (MESH:D013927), COVID (MESH:D000086382), infected (MESH:D007239), endothelial injury (MESH:D057772), renal dysfunction (MESH:D007674), systemic (MESH:D015619), Post-COVID (MESH:D000094024), complications (MESH:D008107), Chronic inflammation (MESH:D007249), diabetes mellitus (MESH:D003920), endothelial dysfunction (MESH:D014652), autoimmunity (MESH:D001327), respiratory insufficiency (MESH:D012131), fatigue (MESH:D005221), ME/CFS (MESH:D015673)
- **Chemicals:** superoxide (MESH:D013481), D (MESH:D003903), Cupric (-), MDA (MESH:D008315), reactive oxygen species (MESH:D017382), adenosine (MESH:D000241)
- **Species:** Staphylococcus aureus (species) [taxon 1280], Homo sapiens (human, species) [taxon 9606], Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12909393/full.md

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Source: https://tomesphere.com/paper/PMC12909393