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Related Experiment Video

Updated: Jul 4, 2026

Passive Administration of Monoclonal Antibodies Against H. capsulatum and Others Fungal Pathogens

Passive Administration of Monoclonal Antibodies Against H. capsulatum and Others Fungal Pathogens

Published on: February 14, 2011

Histoplasma capsulatum pathogenesis: making a lifestyle switch.

Eric D Holbrook¹, Chad A Rappleye

¹Department of Microbiology, Ohio State University, Columbus, OH 43210, United States.

Current Opinion in Microbiology

|June 25, 2008

Summary

Histoplasma's dimorphism, regulated by DRK1 and RYP1, is crucial for virulence. Key virulence factors like HSP60, alpha-glucans, CBP, and YPS3 enable host cell interaction and pathogen survival.

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Last Updated: Jul 4, 2026

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Immunometabolic Circuits in Infection for Advancing Host Directed Therapies

Immunometabolic Circuits in Infection for Advancing Host Directed Therapies

Published on: September 13, 2024

Area of Science:

Mycology
Pathogenesis
Molecular Biology

Background:

Histoplasma exhibits dimorphism, switching between mold and yeast forms, a critical factor for its virulence.
This morphological transition is essential for the fungus to establish infection and cause disease in hosts.

Purpose of the Study:

To elucidate the molecular mechanisms underlying Histoplasma dimorphism and its role in virulence.
To identify specific virulence factors involved in the yeast-phase program and host-pathogen interactions.

Main Methods:

Investigated the roles of dimorphism regulating kinase DRK1 and RYP1 in thermal transition.
Analyzed the function of surface-localized HSP60, alpha-glucan polysaccharides, and secreted CBP in host interaction.
Examined the contribution of YPS3 to dissemination in specific Histoplasma strains.

Main Results:

DRK1 and RYP1 mediate the transition to the yeast-phase, activating virulence-associated genes.
Surface HSP60 aids yeast attachment, while alpha-glucans mask beta-glucans, evading immune detection.
CBP facilitates intracellular growth within macrophages, and YPS3 promotes dissemination.

Conclusions:

Histoplasma dimorphism is a key virulence determinant, orchestrated by specific regulatory and effector molecules.
The yeast-phase program employs diverse strategies, including immune evasion and host cell manipulation, to ensure pathogen survival and spread.