A Gammaherpesvirus Uses Alternative Splicing to Regulate Its Tropism and Its Sensitivity to Neutralization.

Machiels, Benedicte, Stevenson, Philip G., Vanderplasschen, Alain and Gillet, Laurent (2013) A Gammaherpesvirus Uses Alternative Splicing to Regulate Its Tropism and Its Sensitivity to Neutralization.. PLoS Pathogens, 9 10: e1003753-e1003753. doi:10.1371/journal.ppat.1003753


Author Machiels, Benedicte
Stevenson, Philip G.
Vanderplasschen, Alain
Gillet, Laurent
Title A Gammaherpesvirus Uses Alternative Splicing to Regulate Its Tropism and Its Sensitivity to Neutralization.
Journal name PLoS Pathogens   Check publisher's open access policy
ISSN 1553-7366
Publication date 2013-10-01
Year available 2013
Sub-type Article (original research)
DOI 10.1371/journal.ppat.1003753
Open Access Status DOI
Volume 9
Issue 10
Start page e1003753
End page e1003753
Total pages 14
Place of publication San Francisco, CA United States
Publisher Public Library of Science
Collection year 2013
Language eng
Formatted abstract
Human gammaherpesviruses are associated with the development of lymphomas and epithelial malignancies. The heterogeneity of these tumors reflects the ability of these viruses to route infection to different cell types at various stages of their lifecycle. While the Epstein Barr virus uses gp42 – human leukocyte antigen class II interaction as a switch of cell tropism, the molecular mechanism that orientates tropism of rhadinoviruses is still poorly defined. Here, we used bovine herpesvirus 4 (BoHV-4) to further elucidate how rhadinoviruses regulate their infectivity. In the absence of any gp42 homolog, BoHV-4 exploits the alternative splicing of its Bo10 gene to produce distinct viral populations that behave differently based on the originating cell. While epithelial cells produce virions with high levels of the accessory envelope protein gp180, encoded by a Bo10 spliced product, myeloid cells express reduced levels of gp180. As a consequence, virions grown in epithelial cells are hardly infectious for CD14+ circulating cells, but are relatively resistant to antibody neutralization due to the shielding property of gp180 for vulnerable entry epitopes. In contrast, myeloid virions readily infect CD14+ circulating cells but are easily neutralized. This molecular switch could therefore allow BoHV-4 to promote either, on the one hand, its dissemination into the organism, or, on the other hand, its transmission between hosts.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Chemistry and Molecular Biosciences
 
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Created: Mon, 23 Mar 2015, 21:54:27 EST by Mrs Louise Nimwegen on behalf of School of Chemistry & Molecular Biosciences