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April 3, 2026Pathogens0 citationsOpen Access

Orientia tsutsugamushi Alters Mitochondrial Function and Selectively Associates with VDAC

SSSavannah E. SanchezTCTravis J. ChiarelliJBJohn S. Billingsley

Key Points

  • The study aims to examine how Orientia tsutsugamushi impacts mitochondrial function during infection.
  • Conducted confocal and structured illumination microscopy to visualize bacterial and mitochondrial interactions.
  • Assessed mitochondrial enzyme activity to determine impairment.
  • Analyzed the presence and colocalization of VDAC proteins with Orientia tsutsugamushi.
  • Utilized immunosignaling to identify VDAC paralogs in bacterial membranes.
  • Orientia tsutsugamushi induces impaired mitochondrial enzymatic activity.
  • Mitochondrial structural abnormalities are observed without a decrease in overall abundance.
  • A selective association is found between Orientia tsutsugamushi and VDAC1/VDAC3, but not VDAC2.

Abstract

Orientia tsutsugamushi is an obligate intracellular alphaproteobacterium and the causative agent of the potentially fatal rickettsiosis, scrub typhus. During infection, O. tsutsugamushi replicates exclusively in the eukaryotic cytosol near mitochondria and alters host metabolic pathways governed by mitochondria. We report that O. tsutsugamushi induces mitochondrial enzymatic impairment and structural abnormalities without altering mitochondrial abundance or the levels of proteins that maintain mitochondrial homeostasis. Confocal and structured illumination microscopy revealed a selective spatial association between O. tsutsugamushi and the mitochondrial membrane protein, voltage-dependent anion channel (VDAC) but not other mitochondrial proteins. Immunosignal for VDAC paralogs 1 and 3 colocalized with cytosolic O. tsutsugamushi organisms whereas VDAC2 did not. Additionally, the antibody specific for VDAC1 and VDAC3 detected proteins of the expected sizes in Orientia membrane fractions. These findings indicate that O. tsutsugamushi negatively impacts mitochondrial function without overt organelle loss and selectively associates with VDAC1/VDAC3.

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Cite This Study

Sanchez et al. (2026) studied this question.

synapsesocial.com/papers/69cf5d1f5a333a821460abffhttps://doi.org/10.3390/pathogens15040372
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