Many arboviruses can cause viral encephalitis, leading to substantial morbidity and mortality. We previously demonstrated that targeting immune cell migration can improve outcome in a mouse model of lethal arboviral encephalitis. Yet, immune cell migration to and within the brain is incompletely understood. The first and most abundant immune cells recruited to the encephalitic brain are monocytes, which play a role in antiviral defence but also neuropathologies. Their mobilisation from bone marrow (BM) depends primarily on the chemokine receptor CCR2, which is encoded within a locus with CCR1, CCR3 and CCR5. Notably, CCR5 deficiency in humans is associated with increased morbidity during viral encephalitis. Using chemokine receptor reporter mice, we observed lower CCR2 expression by monocytes in the brain compared to BM and blood (46% vs 85-97%), whilst CCR5 expression was higher (28% vs 2-5%). To determine the importance of CCR2 for monocyte migration to the encephalitic brain, we infected mice with Semliki Forest Virus and compared monocyte migration in mice lacking CCR1/2/3/5, or deficient for CCR1/3/5 but not CCR2. Full locus deletion reduced the presence of monocytes and their macrophage progeny in the encephalitic brain by 97%, a defect fully restored by re-establishing CCR2 alone. RNAseq analysis of mixed glial/neuronal cell cultures treated with interferon-beta, a key antiviral cytokine, demonstrated all brain cell types expressed chemotactic cytokines involved in monocyte recruitment. Conclusions. CCR2 expression is critical for monocyte migration to the inflamed brain. We hypothesise CCR5 is important for movement within the brain, ongoing studies are testing this.