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Murine CMV (MCMV) colonizes the salivary glands for long-term shedding, and reaches them via CD11c<jats:sup>+<\/jats:sup> 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. 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