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Molecular and evolutionary basis for survival, its failure, and virulence factors of the zoonotic nematode Anisakis pegreffii*

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60077344%3A_____%2F21%3A00555205" target="_blank" >RIV/60077344:_____/21:00555205 - isvavai.cz</a>

  • Výsledek na webu

    <a href="https://www.sciencedirect.com/science/article/pii/S0888754321002500?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0888754321002500?via%3Dihub</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.ygeno.2021.06.032" target="_blank" >10.1016/j.ygeno.2021.06.032</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Molecular and evolutionary basis for survival, its failure, and virulence factors of the zoonotic nematode Anisakis pegreffii*

  • Popis výsledku v původním jazyce

    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.

  • Název v anglickém jazyce

    Molecular and evolutionary basis for survival, its failure, and virulence factors of the zoonotic nematode Anisakis pegreffii*

  • Popis výsledku anglicky

    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.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    10603 - Genetics and heredity (medical genetics to be 3)

Návaznosti výsledku

  • Projekt

  • Návaznosti

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Ostatní

  • Rok uplatnění

    2021

  • Kód důvěrnosti údajů

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Údaje specifické pro druh výsledku

  • Název periodika

    Genomics

  • ISSN

    0888-7543

  • e-ISSN

    1089-8646

  • Svazek periodika

    113

  • Číslo periodika v rámci svazku

    5

  • Stát vydavatele periodika

    US - Spojené státy americké

  • Počet stran výsledku

    15

  • Strana od-do

    2891-2905

  • Kód UT WoS článku

    000688402900001

  • EID výsledku v databázi Scopus

    2-s2.0-85109199552