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Taxonomic group: fungi / Ascomycota (Phylum: Ascomycota)
Associated disease: infection due to Aspergillus [ICD11: XN0WC

]

NCBI PubMed ID: 31671548
Publication DOI: 10.3390/cells8111348
Journal NLM ID: 101600052
Publisher: Basel, Switzerland: MDPI
Correspondence: Lee DJ <danielle.lee2

griffithuni.edu.au>; O'Donnell H <holly.odonnell

griffithuni.edu.au>; Routier FH <Routier.francoise

mh-hannover.de>Tiralongo J <j.tiralongo

griffith.edu.au>; Haselhorst T <t.haselhorst

griffith.edu.au>
Institutions: Institute for Glycomics, Griffith University, Queensland, Australia, Member of Fraunhofer International Consortium for Anti-Infective Research (iCAIR), Hannover, Germany, Department of Clinical Biochemistry OE4340, Hannover Medical School, Hannover, Germany

Invasive fungal infections (IFI) are an increasing threat to the developing world, with fungal spores being ubiquitous and inhaled every day. Some fungal species are commensal organisms that are part of the normal human microbiota, and, as such, do not pose a threat to the immune system. However, when the natural balance of this association is disturbed or the host's immune system is compromised, these fungal pathogens overtake the organism, and cause IFI. To understand the invasiveness of these pathogens and to address the growing problem of IFI, it is essential to identify the cellular processes of the invading organism and their virulence. In this review, we will discuss the prevalence and current options available to treat IFI, including recent reports of drug resistance. Nevertheless, the main focus of this review is to describe the glycobiology of human fungal pathogens and how various components of the fungal cell wall, particularly cell wall polysaccharides and glycoconjugates, are involved in fungal pathogenicity, their biosynthesis and how they can be potentially exploited to develop novel antifungal treatment options. We will specifically describe the nucleotide sugar transporters (NSTs) that are important in fungal survival and suggest that the inhibition of fungal NSTs may potentially be useful to prevent the establishment of fungal infections.

UDP-galactofuranose, Candida, Aspergillus, GDP-mannose, Cryptococcus, nucleotide sugar transporter, immunosuppression, invasive fungal infection, UDP-glucuronic acid, UDP-xylose

Structure type: structural motif or average structure
Location inside paper: Fig. 2, f
Compound class: polysaccharide, galactomannan
Contained glycoepitopes: IEDB_130701,IEDB_136095,IEDB_136104,IEDB_137472,IEDB_140116,IEDB_141793,IEDB_141795,IEDB_141828,IEDB_141829,IEDB_141830,IEDB_141831,IEDB_141832,IEDB_141833,IEDB_143632,IEDB_144983,IEDB_149137,IEDB_152206,IEDB_153220,IEDB_153762,IEDB_164480,IEDB_190606,IEDB_76933,IEDB_885812,IEDB_983930,SB_136,SB_191,SB_196,SB_198,SB_44,SB_67,SB_72

NCBI Taxonomy refs (TaxIDs): 5052
Reference(s) to other database(s): GTC:G97250CE
Show glycosyltransferases

There is only one chemically distinct structure:

*OC[C@H]1O[C@H](OC[C@H]2O[C@H](O[C@H]3[C@@H](O[C@@H]4O[C@@H]([C@@H](CO)O[C@@H]5O[C@@H]([C@@H](CO)O[C@@H]6O[C@@H]([C@@H](CO)O[C@@H]7O[C@@H]([C@H](O)CO)[C@H](O)[C@H]7O)[C@H](O)[C@H]6O)[C@H](O)[C@H]5O)[C@H](O)[C@H]4O)[C@H](O)[C@@H](CO)O[C@@H]3O[C@H]3[C@@H](O)[C@H](O)[C@@H](CO)O[C@@H]3O[C@@H]3[C@@H](OC[C@H]4O[C@H](*)[C@@H](O)[C@@H](O)[C@@H]4O)O[C@H](CO)[C@@H](O)[C@@H]3O[C@@H]3O[C@@H]([C@@H](CO)O[C@@H]4O[C@@H]([C@@H](CO)O[C@@H]5O[C@@H]([C@@H](CO)O[C@@H]6O[C@@H]([C@H](O)CO)[C@H](O)[C@H]6O)[C@H](O)[C@H]5O)[C@H](O)[C@H]4O)[C@H](O)[C@H]3O)[C@@H](O)[C@@H](O)[C@@H]2O)[C@@H](O)[C@@H](O)[C@@H]1O

SVG MW SMILES 3D mol Ionize

Warning = sub-repeat ending at bDGalf: unknown unit count was assumed to be 3
Warning = sub-repeat ending at bDGalf: unknown unit count was assumed to be 3