Anisakiasis: A Decade of Molecular and Diagnostic Advancements (2015-2026).

Anisakiasis is caused by ingestion of third-stage larvae (L3) of Anisakis in fish. The last decade has improved our understanding of Anisakis and its clinical manifestations, driven by advancements in high-throughput "omics" techniques and molecular diagnostics. This review summarizes major advancements, focusing on molecular mechanisms underlying its pathogenesis, host-pathogen interactions and novel diagnostic approaches. Taxonomical revisions have refined the Anisakis genus, reclassifying several species into Skrjabinisakis and Peritrachelius. Research has highlighted the critical role of Anisakis extracellular vesicles in modulating host immunity. Significant diagnostic breakthroughs include the use of the IgA/IgG4 ratio and antibody avidity profiling to differentiate gastroallergic anisakiasis from chronic urticaria. Identification of α-Gal epitopes in L3 suggests a novel link to α-Gal syndrome and red meat allergy. Ani s 13 and Ani s 14 have been identified as new major allergens, although Ani s 7 remains the gold standard for serological diagnosis. Modern systems biology is revealing how larvae adapt to their host environments, including thermal stress and glucose availability. Finally, emerging evidence suggests potential links between chronic Anisakis exposure and pathologies like cancer and sepsis. These advancements underscore the necessity of global clinical awareness and the potential for Anisakis-derived molecules as templates for future immunotherapies.