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Title: Contribution of N-linked glycans on HSV-2 gB to cell–cell fusion and viral entry

HSV-2 is the major cause of genital herpes and its infection increases the risk of HIV-1 acquisition and transmission. HSV-2 glycoprotein B together with glycoproteins D, H and L are indispensable for viral entry, of which gB, as a class III fusogen, plays an essential role. HSV-2 gB has seven potential N-linked glycosylation (N-CHO) sites, but their significance has yet to be determined. For the first time, we systematically analyzed the contributions of N-linked glycans on gB to cell–cell fusion and viral entry. Our results demonstrated that, of the seven potential N-CHO sites on gB, mutation at N390, N483 or N668 decreased cell–cell fusion and viral entry, while mutation at N133 mainly affected protein expression and the production of infectious virus particles by blocking the transport of gB from the endoplasmic reticulum to Golgi. Our findings highlight the significance of N-linked glycans on HSV-2 gB expression and function. - Highlights: • N-linked glycan at N133 is important for gB intracellular trafficking and maturation. • N-linked glycans at N390, N483 and N668 on gB are necessary for optimal cell–cell fusion. • N-linked glycans at N390, N483 and N668 on gB are necessary for optimal viral entry.
Authors:
 [1] ;  [2] ;  [1] ; ; ; ;  [1] ;  [2] ;  [1] ;  [3] ;  [1] ;  [1] ;  [4]
  1. State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071 (China)
  2. (China)
  3. Soochow University, Institutes of Biology and Medical Sciences, Suzhou 215123 (China)
  4. (United Kingdom)
Publication Date:
OSTI Identifier:
22470186
Resource Type:
Journal Article
Resource Relation:
Journal Name: Virology; Journal Volume: 483; Other Information: Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; AIDS VIRUS; CHANNELING; ENDOPLASMIC RETICULUM; GLYCOPROTEINS; HAZARDS; MUTATIONS; PARTICLES; TRANSMISSION