Journal
ANTIVIRAL THERAPY
Volume 20, Issue 3, Pages 257-259Publisher
INT MEDICAL PRESS LTD
DOI: 10.3851/IMP2907
Keywords
-
Categories
Funding
- NIAID NIH HHS [R01 AI104636, R01 AI113267, AI232758] Funding Source: Medline
Ask authors/readers for more resources
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
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available