Abstract
Talaromyces (Penicillium) marneffei is an important opportunistic fungal pathogen. It causes disseminated infection in immunocompromised patients especially in Southeast Asian countries. The pathogenicity of T. marneffei depends on the ability of the fungus to survive the killing process and replicate inside the macrophage. Major stresses inside the phagosome of macrophages are heat, oxidative substances and nutrient deprivation. The coping strategies of this pathogen with these stresses are under investigation. This paper summarizes factors relating to the stress responses that contribute to the intracellular survival of T. marneffei. These include molecules in the MAP signal transduction cascade, heat shock proteins, antioxidant enzymes and enzymes responsible in nutrient retrieval. There is speculation that the ability of T. marneffei to withstand these defenses plays an important role in its pathogenicity.
Highlights
Adaptation to macrophage killing by Talaromyces marneffeiTalaromyces (Penicillium) marneffei is an important opportunistic fungal pathogen. It causes disseminated infection in immunocompromised patients especially in Southeast Asian countries
The ultrastructure study demonstrated the fate of Talaromyces marneffei after engulfment into the phagosome of macrophages
The conidia must be able to adapt to conditions of heat, oxidative/nitrosative stress and nutrient deprivation found inside the phagosomes of macrophages
Summary
Talaromyces (Penicillium) marneffei is an important opportunistic fungal pathogen. It causes disseminated infection in immunocompromised patients especially in Southeast Asian countries. Some of the genes relating to oxidative and heat stress responses have been reported, for example, genes coding for catalaseperoxidase (CpeA) [34] and Hsp30 [35] Their transcripts were found to accumulate in the conidia and are upregulated in the yeast form, suggesting the potential role of these proteins in the yeast pathogenic phase of this fungus. The sakA is involved in a wide variety of cell activities including yeast morphogenesis, sporulation and red pigment formation [61] Both sakA and atfA gene deletion resulted in the decreased survival of conidia inside human macrophage cell line, suggesting they may have a role in protecting the conidia from macrophage killing [59,60].
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