Omics landscapes of hepatic echinococcosis: bulk foundations, emerging single-cell studies, and analytical considerations.

Hepatic echinococcosis (HE) is a major zoonotic disease in endemic regions, caused predominantly by Echinococcus granulosus sensu lato (cystic echinococcosis, CE) and Echinococcus multilocularis (alveolar echinococcosis, AE). Lesion progression reflects a prolonged host-parasite stalemate in which immunoregulation converges with angiogenesis and fibrovascular remodeling to enable chronic persistence, yet the cellular drivers and niche-specific interactions that sustain these lesions remain incompletely defined. While bulk omics has established a valuable foundation by delineating global perturbations in immune pathways, vascular programs, and extracellular matrix remodeling, these approaches average signals across heterogeneous lesions and adjacent liver, limiting the resolution of discrete cell states and intercellular communication that underpin persistence. Recent advances in single-cell RNA sequencing (scRNA-seq) and emerging spatial transcriptomics (ST) are beginning to overcome these limitations by enabling cell-resolved, niche-aware profiling of HE tissues. Early applications in HE have implicated late-stage expansion of SPP1+ macrophages, exhausted T-cell programs, and pro-angiogenic myeloid-endothelial crosstalk, providing a more mechanistic and spatially grounded view of fibrovascular remodeling and chronic inflammation. In this review, we synthesize key insights from scRNA-seq and ST studies of HE lesions and adjacent liver, discuss analytical considerations that are particularly relevant to fibrotic and necrotic tissues, and emphasize stage-aware and lesion-zone-aware interpretation. Taken together, we propose an integrative framework that links cell-state diversity to spatial context to prioritize actionable pathways and guide next-generation multi-omic investigations of HE.