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Intracellular parasitism by Histoplasma capsulatum: fungal virulence and calcium dependence

T S Sebghati1, J T Engle, W E Goldman

  • 1Department of Molecular Microbiology, Campus Box 8230, Washington University School of Medicine, St. Louis, MO 63110, USA.

Science (New York, N.Y.)
|November 18, 2000
PubMed

Insights

Histoplasma capsulatum yeasts require calcium for growth and virulence. Disrupting the calcium-binding protein 1 (CBP1) gene prevented fungal growth in low-calcium conditions and reduced disease severity in a mouse model.

Area of Science:

  • Mycology
  • Infectious Diseases
  • Molecular Biology

Background:

  • Histoplasma capsulatum causes the most common fungal respiratory disease in the U.S.
  • This dimorphic fungus shifts from soil mold to parasitic yeast upon inhalation.
  • Only the yeast form thrives in low-calcium environments and secretes a calcium-binding protein (CBP).

Purpose of the Study:

  • To investigate the link between calcium limitation and H. capsulatum's parasitic capabilities.
  • To disrupt the CBP1 gene in H. capsulatum and assess its impact on fungal growth and virulence.

Main Methods:

  • A telomeric linear plasmid was used to disrupt the CBP1 gene.
  • A two-step genetic selection strategy was employed for gene disruption.
  • cbp1 mutant yeasts were tested for growth in calcium-limited conditions.
  • Macrophage destruction and proliferation in a mouse infection model were assessed.

Main Results:

  • The cb p1 mutant yeasts failed to grow when deprived of calcium.
  • The cb p1 mutant yeasts exhibited reduced ability to destroy macrophages in vitro.
  • Pulmonary infection progression was significantly impaired in the mouse model with the cb p1 mutant.

Conclusions:

  • Calcium-binding protein 1 (CBP1) is essential for H. capsulatum yeast growth under calcium-limiting conditions.
  • CBP1 plays a critical role in the intracellular parasitic mechanisms of H. capsulatum, including macrophage destruction and virulence.
  • Targeting CBP1 may represent a novel therapeutic strategy for histoplasmosis.

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