Mice were infected with HV-68, with viral latency being established in these animals. At varying times post-infection, cells were isolated for detection of viral genomes, phenotyping of myeloid cell populations, and ex vivo analysis of suppressor activity of myeloid cells.CD11b？+？Gr-1+ myeloid cells accumulated in the spleens, but not the bone marrow, of HV-68 infected mice. These cells were predominantly Gr-1+ Ly-6？G+, and could be found to contain viral genomes. Increased levels of serum S100A8/A9 produced during viral infection were consistent with the expansion of these CD11b？+？Gr-1+ myeloid cells. Despite their expansion, these cells exhibited no increased arginase 1 or iNOS activity, and did not have the ability to suppress anti-CD3 antibody activated T lymphocyte responses.We concluded that HV-68 infection was capable of expanding a population of myeloid cells which were phenotypically similar to MDSC. However these cells were not sufficiently activated during the establishment of viral latency to actively suppress T cell responses.