BAFF receptor deficiency limits gammaherpesvirus infection

Frederico, Bruno, May, Janet S., Efstathiou, Stacey and Stevenson, Philip G. (2014) BAFF receptor deficiency limits gammaherpesvirus infection. Journal of Virology, 88 8: 3965-3975. doi:10.1128/JVI.03497-13

Author Frederico, Bruno
May, Janet S.
Efstathiou, Stacey
Stevenson, Philip G.
Title BAFF receptor deficiency limits gammaherpesvirus infection
Journal name Journal of Virology   Check publisher's open access policy
ISSN 1098-5514
Publication date 2014-04
Year available 2014
Sub-type Article (original research)
DOI 10.1128/JVI.03497-13
Open Access Status DOI
Volume 88
Issue 8
Start page 3965
End page 3975
Total pages 11
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Collection year 2015
Language eng
Formatted abstract
Lymphocyte colonization by gammaherpesviruses (γHVs) is an important target for cancer prevention. However, how it works is not clear. Epstein-Barr virus drives autonomous B cell proliferation in vitro but in vivo may more subtly exploit the proliferative pathways provided by lymphoid germinal centers (GCs). Murid herpesvirus 4 (MuHV-4), which realistically infects inbred mice, provides a useful tool with which to understand further how a γHV colonizes B cells in vivo. Not all γHVs necessarily behave the same, but common events can with MuHV-4 be assigned an importance for host colonization and so a potential as therapeutic targets. MuHV-4-driven B cell proliferation depends quantitatively on CD4+ T cell help. Here we show that it also depends on T cell-independent survival signals provided by the B cell-activating factor (BAFF) receptor (BAFF-R). B cells could be infected in BAFF-R-/- mice, but virus loads remained low. This corresponded to a BAFF-R dependent defect in GC colonization. The close parallels between normal, antigen-driven B cell responses and virus infected B cell proliferation argue that in vivo, γHVs mostly induce infected B cells into normal GC reactions rather than generating large numbers of autonomously proliferating blasts.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
School of Chemistry and Molecular Biosciences
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