Open AccessHuman cytomegalovirus US28 allows dendritic cell exit from lymph nodes
Author(s) -
Helen E. Farrell,
Kimberley Bruce,
Jiawei Ma,
Nicholas Davis-Poynter,
Philip G. Stevenson
Publication year - 2018
Publication title -
journal of general virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.55
H-Index - 167
eISSN - 1465-2099
pISSN - 0022-1317
DOI - 10.1099/jgv.0.001154
Subject(s) - biology , human cytomegalovirus , virology , cytomegalovirus , receptor , extravasation , immunology , microbiology and biotechnology , ctl* , immune system , virus , herpesviridae , viral disease , genetics , cd8
Human cytomegalovirus (HCMV) colonizes blood-borne dendritic cells (DCs). They express US28, a viral G protein-coupled receptor (GPCR). In vitro functions have been described for US28, but how it contributes to host colonization has been unclear. The murine CMV (MCMV) M33 GPCR promotes DC recirculation. We show that US28 shares this function. Thus, DC recirculation is also available to HCMV via US28, and inhibiting US28 G protein-dependent signalling has the potential to reduce systemic infection. We show that M33 also promotes systemic infection through infected DC extravasation.