A murid gamma-herpesviruses exploits normal splenic immune communication routes for systemic spread
- Author(s)
- Frederico, B; Chao, B; May, JS; Belz, GT; Stevenson, PG;
- Details
- Publication Year 2014-04-09,Volume 15,Issue #4,Page 457-70
- Journal Title
- Cell host & microbe
- Publication Type
- Journal Article
- Abstract
- Gamma-herpesviruses (gammaHVs) are widespread oncogenic pathogens that chronically infect circulating lymphocytes. How they subvert the immune check-point function of the spleen to promote persistent infection is not clear. We show that Murid Herpesvirus-4 (MuHV-4) enters the spleen by infecting marginal zone (MZ) macrophages, which provided a conduit to MZ B cells. Relocation of MZ B cells to the white pulp allowed virus transfer to follicular dendritic cells. From here the virus reached germinal center B cells to establish persistent infection. Mice lacking MZ B cells, or treated with a sphingosine-1-phosphate receptor agonist to dislocate them, were protected against MuHV-4 colonization. MuHV-4 lacking ORF27, which encodes a glycoprotein necessary for efficient intercellular spread, could infect MZ macrophages but was impaired in long-term infection. Thus, MuHV-4, a gammaHV, exploits normal immune communication routes to spread by serial lymphoid/myeloid exchange.
- Publisher
- Cell Press
- Research Division(s)
- Molecular Immunology
- Publisher's Version
- https://doi.org/10.1016/j.chom.2014.03.010
- Terms of Use/Rights Notice
- Copyright © 2014 Elsevier Inc. All rights reserved.
Creation Date: 2014-04-16 08:43:40