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The cellular sites and mechanisms of human cyto-megalovirus (HCMV) latency are still poorly defined. Although evidence suggests that peripheral blood monocytes are one site of latency in the healthy carrier, it is unlikely that monocytes represent a site of primary HCMV infection. Consequently, we have analysed CD34 + bone marrow progenitors, pre-cursors of monocytes, to determine whether they are a site of HCMV carriage in normal virus carriers. For the first time, we demonstrate the presence of endogenous HCMV within bone marrow pro-genitors in the absence of HCMV lyric gene ex-pression. These findings are consistent with pre-vious evidence showing that the permissiveness of myeloid cells for HCMV is critically dependent o