Open AccessMurine cytomegalovirus disseminates independently of CX3CR1, CCL2 or its m131/m129 chemokine homologue
Author(s) -
Helen E. Farrell,
Kimberley Bruce,
Alec Redwood,
Philip G. Stevenson
Publication year - 2019
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.0.001333
Subject(s) - cx3cr1 , biology , salivary gland , immunology , chemokine receptor , cd11c , chemokine , virology , ccl17 , inflammation , gene , phenotype , biochemistry
Cytomegaloviruses (CMVs) use myeloid cells to move within their hosts. Murine CMV (MCMV) colonizes the salivary glands for long-term shedding, and reaches them via CD11c + infected cells. A need to recruit patrolling monocytes for systemic spread has been proposed, based on poor salivary gland infection in fractalkine receptor (CX3CR1)-deficient mice. We found no significant CX3CR1 dependence of salivary gland infection. CCL2 and the viral m131/m129 chemokine homologue were also redundant for acute MCMV spread, arguing against a need for inflammation or infection to recruit additional monocytes to the entry site. M131/m129 promoted salivary gland infection, but only after the initial seeding of infected cells to this site. Our data support the idea that MCMV disseminates by infecting and mobilizing tissue-resident dendritic cells.