LAUSR

Invasive mycotic infections account for an unacceptably high mortality rates in humans. These infections are initiated by the fungal cell wall which mediates host-fungi interactions. The cell wall is fused to the physiology of fungi, and it is involved in essential functions in the entire cell functionality. Components of the cell wall are synthesised and modified in the cell wall space by the activities of cell wall proteins through a range of signalling pathways that have only been described in many fungi, therefore making them suitable drug targets. The echinocandins class of cell wall-active drugs block cell wall β-1,3-glucan biosynthesis through inhibiting the catalytic subunit of the synthetic protein complex. Resistance to echinocandins can be through the acquisition of single nucleotide polymorphisms and/or through activation of cell wall signalling pathways resulting in altered cell wall proteome and elevated chitin content in the cell wall. Countering the cell wall remodelling process will enhance the effectiveness of β-1,3-glucan-active antifungal agents. Cell surface proteins are also important antifungal targets which can be used to develop rapid and robust diagnostics and more effective therapeutics. The cell wall remains a crucial target in fungi that needs to be harnessed to combat mycotic infections.