Fungal immune evasion articles from across Nature Portfolio

Bivalent histone modifications control various cellular processes in eukaryotes. Here, the authors report that a fungal pathogen deploys bivalent histone modification to fine-tune the expression of BCG1, thereby facilitating successful infection and host immunity evasion.

Here the authors find that surface antigenic variation of the human pathogenic fungus Pneumocystis jirovecii involves mosaicism and reassortment of the repertoire of 80 genes present in each strain, from which single genes are retrieved for mutually exclusive expression.

The study explores immune evasion mechanisms of T. marneffei infection, highlighting the role of alternative splicing (AS). T. marneffei triggers the upregulation of NCOR2-013, inhibiting pro-inflammatory cytokine production via histone acetylation. TUT1 regulates NCOR2-013, contributing to immune evasion. This sheds light on T. marneffei’s immune evasion at the molecular level, offering potential talaromycosis therapy targets.

Plant PR-1 proteins participate in defense responses against pathogens. Here, the authors show that PR-1-like proteins from the plant pathogenic fungus Ustilago maydis are important for virulence by detecting plant-derived phenolics and modulating plant PR-1-mediated defenses.

Metabolic flexibility allows fungi to invade hostile niches. Here, Liu et al. dissect the molecular mechanisms by which Candida albicans upregulates virulence-enabling alternative oxidase expression in response to host-relevant respiratory stresses.

Real-time imaging of fungal infection and tissue clearing in the wax moth, Galleria mellonella, help evaluate the role of melanin in the insect host immune response to fungal pathogens.

The mammalian immune system has evolved to tolerate commensal microbes that inhabit our mucosal surfaces. Two recent studies explore how intestinal immunity achieves this state of tolerance and show that IgA enforces commensalism of pathobiont Candida species.

Plants respond to microbial attack with a lethal burst of reactive oxygen species. How then, do pathogens successfully invade plants? Unexpectedly, a link between primary metabolism and suppression of plant immunity allows the rice blast fungus Magnaporthe oryzae to grow in such a hostile environment.

Growth of Candida albicans on different host carbon sources reveals that the cell wall is a live organelle that can respond to alterations in the environment by masking a cell surface epitope to protect the fungal cell from the host immune response.

This month's Genome Watch looks at how genome sequence analysis aids our understanding of pathogen survival within hosts.