To sialylate, or not to sialylate: that is the question.
Most oropharyngeal pathogens express sialic acid units on their surfaces, mimicking the sialyl-rich mucin layer coating epithelial cells and the glycoconjugates present on virtually all host cell surfaces and serum proteins. Unlike the host's cells, which synthesize sialic acids endogenously, several microbial pathogens use truncated sialylation pathways. How microorganisms regulate sialic acid metabolism to ensure an adequate supply of free sugar for surface remodeling is a new area of research interest to basic scientists and those focused on the clinical outcome of the host-pathogen interaction.
Vimr
Eric
E
Division of Microbiology and Immunology, Dept of Pathobiology, University of Illinois at Urbana-Champaign, 2001 South Lincoln Ave, Urbana, IL 61802, USA. e-vimr@uiuc.edu
Lichtensteiger
Carol
C
D006790:Host-Parasite Interactions; D008954:Models, Biological; D018716:Molecular Mimicry; D019158:N-Acetylneuraminic Acid / Q000378:metabolism*; D009439:Neuraminidase / Q000378:metabolism*; D014774:Virulence / Q000235:genetics
D009439:Neuraminidase; D019158:N-Acetylneuraminic Acid