ArticlemBio2025
Metagenomic and transcriptomic investigation of pediatric acute liver failure cases reveals a common pathway predominated by monocytes.
Article in mBio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Immune mechanisms and pathophysiology of T cell-mediated pediatric acute liver failure (TC-PALF).Hepatology communications · 2026Review
- Adeno-Associated Virus Type 2 and Human Adenovirus Species F Type 41 Co-infection Associated with Acute Severe Hepatitis in Children, California, USA.Emerging infectious diseases · 2026Article
- CD8 TRM-like T cells expressing perforin and IFN-γ define a pediatric activated T-cell acute liver failure endotype.Hepatology communications · 2026Article
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Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In 2022, a cluster of severe childhood hepatitis was detected primarily in Europe and North America, leading to a global alert by the World Health Organization. An association with adeno-associated virus 2 (AAV2) in conjunction with human adenoviruses was found. Five percent of the cases progressed to acute liver failure, necessitating transplantation. The mechanism of disease that accounts for fulminant liver failure in these patients remains incompletely described. An upsurge was observed of in the five total cases of acute liver failure that presented to the Dutch national referral center for pediatric liver transplantation in the spring of 2022. An in-depth molecular analysis of the mechanism of pediatric acute liver failure was performed using targeted transcriptomics and metagenomics to identify any virus present in the cases, immune profile haplotypes, and differentially expressed gene groups. Explanted liver tissue and plasma samples ( IMPORTANCE: Since the appearance of the cluster of pediatric hepatitis of unknown origin in 2022, several groups have reported an association of adenoviruses and AAV2 in a high number of cases in contrast to controls. The adenoviruses detected were heterogeneous in both species-adenovirus C and F-and sequences. The mechanisms of disease that accounts for fulminant liver failure, occurring in 5% of pediatric hepatitis cases, remain incompletely described. The current study adds to previous data by including pediatric acute liver failure cases during the upsurge, enabling the analyses of inflammation expression profiles in cases with different viruses in relation to pediatric controls. This led to the discovery of transcriptome upregulation of monocyte pathways in liver explants from the cases. This inflammatory transcriptomic signature was comparable for AAV2, adenoviruses, and/or herpesviruses-positive transplant cases.
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