@article{mbs:/content/journal/jgv/10.1099/jgv.0.001333, author = "Farrell, Helen E. and Bruce, Kimberley and Redwood, Alec J. and Stevenson, Philip G.", title = "Murine cytomegalovirus disseminates independently of CX3CR1, CCL2 or its m131/m129 chemokine homologue", journal= "Journal of General Virology", year = "2019", volume = "100", number = "12", pages = "1695-1700", doi = "https://doi.org/10.1099/jgv.0.001333", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/jgv.0.001333", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", keywords = "cytomegalovirus", keywords = "salivary glands", keywords = "monocyte", keywords = "chemokine", abstract = "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.", }