ArticleJournal of medical virology2026
Epidemiological and Clinical Characteristics of the Enterovirus D68 Outbreak in Spain in 2024.
Article in Journal of medical virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Corrections and comments
- Erratum issued
Authors and funding
19 authors.
Funding
Abstract
Enterovirus D68 (EV-D68) is a significant cause of respiratory and neurological disease worldwide. In 2024, Spain experienced its largest recorded EV-D68 outbreak, accounting for 37.4% of all typed EV (294/892). This study describes the epidemiological, clinical, and phylogenetic features of EV-D68 infections. Unexpectedly, EV-D68 infections as it seems were more frequent in adults than in children (57.2% vs. 42.8%, p < 0.05), particularly among individuals > 60 years (38.6%). In 84.9% of cases with an EV-D68 infection, EV-D68 was the sole pathogen detected. Respiratory pathologies predominated (91.9%), with bronchospasm/wheezing episodes and bronchiolitis in children, and pneumonia and exacerbations of chronic obstructive pulmonary disease in older adults (p < 0.05). Older patients showed a more severe clinical profile than pediatric patients, including higher hospitalization rates (79% vs. 59%), longer hospital stays (mean, 10.8 vs. 4.9 days), and more comorbidities (50% vs. 31%) (p < 0.01). Phylogenetic analysis revealed two co-circulating lineages with distinct age-related tropisms: B3.3 mainly affected children (88.5%), whereas the novel A2/D1.1 infected adults predominantly (79.6%), particularly ≥ 60 years (49.5%) (p < 0.05). This pattern may reflect lineage-specific amino acid substitutions enhancing immune evasion. Neurological disease occurred in only three patients > 60 years infected by the A2/D1.1 lineage, which contained neurovirulent substitutions (I553L, K835E, and T860N). Results support continued genomic and clinical surveillance of EV-D68.
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