title: Viral resistance of MOGS-CDG patients implies a broad-spectrum strategy against acute virus infections.
abstract: Sadat et al. reported in the 24 April 2014 issue of the New England Journal of Medicine that patients genetically deficient in the gene encoding mannosyl-oligosaccharide glucosidase (MOGS), also known as endoplasmic reticulum (ER) glucosidase I, manifested a severe hypogammaglobulinaemia without clinical evidence of an infectious diathesis. This paradox phenomenon is, at least in part, because the impaired N-linked glycan processing of the patients compromises their ability to support efficient replication and cellular entry of viruses. This finding unambiguously validates ER glucosidases as valuable targets for antiviral agents against a broad-spectrum of enveloped viruses.
authors.affiliation: Department of Microbiology and Immunology, Drexel University College of Medicine, Doylestown, PA, USA.
authors.forename: Jinhong
authors.initials: J
authors.lastname: Chang
authors.forename: Timothy M
authors.initials: TM
authors.lastname: Block
authors.forename: Ju-Tao
authors.initials: JT
authors.lastname: Guo
mesh_terms: D000361:Agammaglobulinemia / Q000235:genetics*; D018981:Congenital Disorders of Glycosylation / Q000276:immunology*; D060467:Disease Resistance / Q000235:genetics*; D005260:Female; D006801:Humans; D008297:Male; D014777:Virus Diseases / Q000276:immunology*; D000520:alpha-Glucosidases / Q000235:genetics*
chemical_list: D000520:alpha-Glucosidases