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Background <p>Amebiasis, which is caused by <i>Entamoeba histolytica</i>, is prevalent worldwide. Clinical presentation varies from asymptomatic infection to life-threatening extraintestinal disease, and the clinical form can change within one infectious episode. It is also known that periodical animal passages are required for maintaining virulence of <i>E. histolytica in vivo</i> model, such as a hamster liver abscess or murine colitis model. However, it remains uncertain whether or for how long virulence induced by environmental stimuli persists during in vitro passage at the clonal level.</p> Results <p>We generated clones from a hamster liver-passaged <i>E. histolytica</i> strain and periodically checked their liver abscess-forming capability during subsequent in vitro passages. We obtained three clones (ALA-1, ALA-5, and ALA-6) that were highly virulent (abscess weight accounting for &gt; 30% of total liver weight in a hamster model). Interestingly, all clones showed reduced virulence, which disappeared completely after 18 months of in vitro passage. Furthermore, the time to loss of virulence varied among the three clones (18, 12, and 6 months for ALA-1, ALA-5, and ALA-6, respectively). Whole-genome sequencing revealed a small number of single nucleotide polymorphisms at different stages in culture, none of which were shared among clones. Transcriptome analysis comparing gene expression between the highly virulent and avirulent states revealed several differentially expressed genes in each clone. However, there was minimal overlap in differentially expressed genes among the three clones, emphasizing the high complexity of virulence expression in <i>E. histolytica</i>.</p> Conclusions <p><i>E. histolytica</i> can transiently adapt their phenotypes according to culture conditions at the clone level. Further studies are needed to clarify the underlying mechanisms of this “protean” infectious disease.</p>

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Entamoeba histolytica clones presenting transient virulent phenotypes: subsequent fate of forcibly induced virulent clones by hamster’s liver abscess model

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  • 发表日期：

    2026年6月15日

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  • Yumiko Saito-Nakano,
  • Shinji Izumiyama,
  • Yasuaki Yanagawa,
  • Seiki Kobayashi,
  • Yuko Umeki,
  • Takashi Makiuchi,
  • Kumiko Nakada-Tsukui,
  • Koji Watanabe

摘要

Background

Amebiasis, which is caused by Entamoeba histolytica, is prevalent worldwide. Clinical presentation varies from asymptomatic infection to life-threatening extraintestinal disease, and the clinical form can change within one infectious episode. It is also known that periodical animal passages are required for maintaining virulence of E. histolytica in vivo model, such as a hamster liver abscess or murine colitis model. However, it remains uncertain whether or for how long virulence induced by environmental stimuli persists during in vitro passage at the clonal level.

Results

We generated clones from a hamster liver-passaged E. histolytica strain and periodically checked their liver abscess-forming capability during subsequent in vitro passages. We obtained three clones (ALA-1, ALA-5, and ALA-6) that were highly virulent (abscess weight accounting for > 30% of total liver weight in a hamster model). Interestingly, all clones showed reduced virulence, which disappeared completely after 18 months of in vitro passage. Furthermore, the time to loss of virulence varied among the three clones (18, 12, and 6 months for ALA-1, ALA-5, and ALA-6, respectively). Whole-genome sequencing revealed a small number of single nucleotide polymorphisms at different stages in culture, none of which were shared among clones. Transcriptome analysis comparing gene expression between the highly virulent and avirulent states revealed several differentially expressed genes in each clone. However, there was minimal overlap in differentially expressed genes among the three clones, emphasizing the high complexity of virulence expression in E. histolytica.

Conclusions

E. histolytica can transiently adapt their phenotypes according to culture conditions at the clone level. Further studies are needed to clarify the underlying mechanisms of this “protean” infectious disease.