Number of the records: 1
Molecular and evolutionary basis for survival, its failure, and virulence factors of the zoonotic nematode Anisakis pegreffii*
- 1.
SYSNO ASEP 0555205 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Molecular and evolutionary basis for survival, its failure, and virulence factors of the zoonotic nematode Anisakis pegreffii* Author(s) Trumbic, Z. (HR)
Hrabar, J. (HR)
Palevich, N. (NZ)
Carbone, V. (NZ)
Mladineo, Ivona (BC-A) RID, ORCIDNumber of authors 5 Source Title Genomics. - : Elsevier - ISSN 0888-7543
Roč. 113, č. 5 (2021), s. 2891-2905Number of pages 15 s. Publication form Print - P Language eng - English Country US - United States Keywords protein ; parasite ; binding ; detoxification ; reconstruction ; identification ; recognition ; carnosinase ; generation ; platform ; Accidental host ; Anisakiasis ; Anisakis spp ; Drug targets modelling ; Paratenic host ; Transcriptomics Subject RIV EB - Genetics ; Molecular Biology OECD category Genetics and heredity (medical genetics to be 3) Method of publishing Limited access Institutional support BC-A - RVO:60077344 UT WOS 000688402900001 EID SCOPUS 85109199552 DOI https://doi.org/10.1016/j.ygeno.2021.06.032 Annotation Parasitism is a highly successful life strategy and a driving force in genetic diversity that has evolved many times over. Accidental infections of non-targeted hosts represent an opportunity for lateral host switches and parasite niche expansion. However, if directed toward organisms that are phylogenetically distant from parasite's natural host, such as humans, it may present a dead-end environment where the parasite fails to mature or is even killed by host immunity. One example are nematodes of Anisakidae family, genus Anisakis, that through evolution have lost the ability to propagate in terrestrial hosts, but can survive for a limited time in humans causing anisakiasis. To scrutinize versatility of Anisakis to infect an evolutionary-distant host, we performed transcriptomic profiling of larvae successfully migrating through the rat, a representative model of accidental human infection and compared it to that of larvae infecting an evolutionary-familiar, paratenic host (fish). In a homeothermic accidental host Anisakis upregulated ribosome-related genes, cell division, cuticle constituents, oxidative phosphorylation, in an unsuccessful attempt to molt to the next stage. In contrast, in the paratenic poikilothermic host where metabolic pathways were moderately upregulated or silenced, larvae prepared for dormancy by triggering autophagy and longevity pathways. Identified differences and the modelling of handful of shared transcripts, provide the first insights into evolution of larval nematode virulence, warranting their further investigation as potential drug therapy targets. Workplace Biology Centre (since 2006) Contact Dana Hypšová, eje@eje.cz, Tel.: 387 775 214 Year of Publishing 2022 Electronic address https://www.sciencedirect.com/science/article/pii/S0888754321002500?via%3Dihub
Number of the records: 1