Host-pathogen interaction – Page 2

Novel endornaviruses infecting Phytophthora cactorum that attenuate vegetative growth, promote sporangia formation and confer hypervirulence to the host oomycete

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Researchers discovered two new viruses infecting a plant-damaging organism called Phytophthora cactorum. When these viruses are present, the organism grows more slowly but becomes more aggressive at infecting plants. The viruses attach to special membranes inside cells and depend on cholesterol-like compounds for their replication. Scientists were able to remove the viruses from infected strains using specialized techniques, allowing them to compare infected and virus-free versions of the organism.

Fungal pathogens and symbionts: Living off the fat of the land

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Certain fungi that live exclusively in or on hosts have evolved a clever survival strategy: they stopped making their own fatty acids and instead steal them from their hosts. This includes fungi that cause pneumonia in immunocompromised patients, yeasts on skin, and beneficial fungi that help plants absorb nutrients from soil. By examining how these fungi scavenge fatty acids from their hosts, scientists hope to develop better treatments and diagnostic tools for fungal infections.

The expression of fungal CotH, human glucose-regulated protein 78 (GRP78), and predicted miRNAs in macrophages and diabetic mice infected with Rhizopus oryzae

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Mucormycosis is a serious fungal infection caused by Rhizopus oryzae that is particularly dangerous for people with diabetes. This study shows that a fungal protein called CotH3 attaches to a human cell receptor called GRP78, allowing the fungus to invade cells more easily in diabetic patients. The research found that diabetes increases GRP78 production, making fungal invasion more likely, while antifungal treatment (liposomal amphotericin B) can reduce the expression of both CotH3 and GRP78.

PTP1B deficiency in myeloid cells increases susceptibility to Candida albicans systemic infection by modulating antifungal immunity

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This research shows that a protein called PTP1B plays an important role in protecting the body against dangerous yeast infections caused by Candida albicans. When this protein is missing from immune cells, mice become much more susceptible to severe fungal infections. The study found that PTP1B helps immune cells called macrophages and neutrophils kill fungi effectively, and when it’s absent, these immune cells work poorly. This discovery suggests that targeting PTP1B could be a new way to help patients fight off serious fungal infections.

Ex Vivo Host Transcriptomics During Cryptococcus neoformans, Cryptococcus gattii, and Candida albicans Infection of Peripheral Blood Mononuclear Cells From South African Volunteers

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Researchers studied how human immune cells respond to three different fungal infections that commonly affect people with weakened immune systems. By examining gene activity in blood cells exposed to these fungi, they discovered that each fungus triggers different immune responses, with Candida albicans causing a much stronger reaction than the two Cryptococcus species. Only one shared immune pathway was activated by all three fungi, suggesting each infection requires different immune mechanisms to fight off. These findings could help develop new treatments for serious fungal infections.

Transcription Factor PFB1 Is Required for the Botrytis cinerea Effector BcSCR1-Mediated Pathogenesis

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Researchers discovered how a fungal disease (grey mould) spreads by identifying a toxic protein it produces that disables a plant’s defense system. The fungal protein BcSCR1 sneaks into plant cells and targets a control switch called PFB1 that normally turns on genes protecting plants from infection. By blocking this control switch, the fungus weakens the plant’s immune defenses and establishes infection more easily.

Circadian clock is critical for fungal pathogenesis by regulating zinc starvation response and secondary metabolism

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Scientists discovered that Fusarium oxysporum, a fungus that causes plant diseases, uses an internal clock system to time its attacks on plants. The fungus is most dangerous at dawn, when it activates special genes to survive the plant’s defenses and produce toxins. By disrupting the fungus’s clock genes, researchers found they could make it harmless. This discovery could lead to new ways to protect crops by targeting the pathogen’s timing system rather than using traditional fungicides.

Research Topic: Host-pathogen interaction

Novel endornaviruses infecting Phytophthora cactorum that attenuate vegetative growth, promote sporangia formation and confer hypervirulence to the host oomycete

Fungal pathogens and symbionts: Living off the fat of the land

The expression of fungal CotH, human glucose-regulated protein 78 (GRP78), and predicted miRNAs in macrophages and diabetic mice infected with Rhizopus oryzae

PTP1B deficiency in myeloid cells increases susceptibility to Candida albicans systemic infection by modulating antifungal immunity

Ex Vivo Host Transcriptomics During Cryptococcus neoformans, Cryptococcus gattii, and Candida albicans Infection of Peripheral Blood Mononuclear Cells From South African Volunteers

Transcription Factor PFB1 Is Required for the Botrytis cinerea Effector BcSCR1-Mediated Pathogenesis

Circadian clock is critical for fungal pathogenesis by regulating zinc starvation response and secondary metabolism