CCR2-expressing leukocytes are required for the progression of fibrosis in models of induced lung injury as well as models of bone marrow transplant (BMT)-related idiopathic pneumonia syndrome (IPS). Infection with murid -herpesvirus-68 (HV-68) results in severe pneumonitis and pulmonary fibrosis following syngeneic BMT; however, the roles that various pro-inflammatory leukocyte populations play in this process remain unclear. Deletion of CCR2 in both non-BMT and BMT mice increased early lytic viral replication and resulted in a reduction in the numbers of lung infiltrating GR1+ / F4/80+, and CXCR1+ cells, while maintaining robust neutrophil infiltration. Similarly, in HV-68 infected CCR2-/- BMT mice, recruitment of monocytes and lymphocytes were reduced whereas neutrophil recruitment was increased compared to WT BMT mice. Interestingly, levels of pro-fibrotic IL-17 were increased in infected CCR2 BMT mice in comparison to WT BMT. Further, an increase in lung-associated collagen was detected even though there was an overall decrease in the number of pro-fibrotic CCR2+ fibrocytes detected in the lungs of CCR2-/- BMT mice. These data indicate that, contrary to most models of fibrosis, deletion of CCR2 offers no protection from -herpesvirus-induced pneumonitis and fibrosis, and indeed, CCR2+ cells play a suppressive role during the development of pulmonary fibrosis following -herpesvirus infection post-BMT by limiting IL-17, and collagen production.