Glycoprotein B cleavage is important for murid herpesvirus 4 to infect myeloid cells

Glauser, Daniel L., Milho, Ricardo, Frederico, Bruno, May, Janet S., Kratz, Anne-Sophie, Gillet, Laurent and Stevenson, Philip G. (2013) Glycoprotein B cleavage is important for murid herpesvirus 4 to infect myeloid cells. Journal of Virology, 87 19: 10828-10842. doi:10.1128/JVI.00709-13


Author Glauser, Daniel L.
Milho, Ricardo
Frederico, Bruno
May, Janet S.
Kratz, Anne-Sophie
Gillet, Laurent
Stevenson, Philip G.
Title Glycoprotein B cleavage is important for murid herpesvirus 4 to infect myeloid cells
Journal name Journal of Virology   Check publisher's open access policy
ISSN 0022-538X
1098-5514
Publication date 2013-10-01
Year available 2013
Sub-type Article (original research)
DOI 10.1128/JVI.00709-13
Open Access Status DOI
Volume 87
Issue 19
Start page 10828
End page 10842
Total pages 15
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Collection year 2013
Language eng
Formatted abstract
Glycoprotein B (gB) is a conserved herpesvirus virion component implicated in membrane fusion. As with many— but not all—herpesviruses, the gB of murid herpesvirus 4 (MuHV-4) is cleaved into disulfide-linked subunits, apparently by furin. Preventing gB cleavage for some herpesviruses causes minor infection deficits in vitro, but what the cleavage contributes to host colonization has been unclear. To address this, we mutated the furin cleavage site (R-R-K-R) of the MuHV-4 gB. Abolishing gB cleavage did not affect its expression levels, glycosylation, or antigenic conformation. In vitro, mutant viruses entered fibroblasts and epithelial cells normally but had a significant entry deficit in myeloid cells such as macrophages and bone marrow-derived dendritic cells. The deficit in myeloid cells was not due to reduced virion binding or endocytosis, suggesting that gB cleavage promotes infection at a postendocytic entry step, presumably viral membrane fusion. In vivo, viruses lacking gB cleavage showed reduced lytic spread in the lungs. Alveolar epithelial cell infection was normal, but alveolar macrophage infection was signifi-cantly reduced. Normal long-term latency in lymphoid tissue was established nonetheless.
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, 21:41:15 EST by Mrs Louise Nimwegen on behalf of School of Chemistry & Molecular Biosciences