Cytomegalovirus (CMV) is a double-stranded DNA virus which can be transmitted by blood transfusion. Its seroprevalence in adults ranges from 40% to 100% depending on geographical and socioeconomic conditions. Seropositive individuals have latent CMV infection with viral DNA present in peripheral blood leucocytes. CMV can be associated with considerable morbidity and mortality in susceptible individuals, e.g. CMV-seronegative bone marrow allograft patients. Evidence, from a number of reports, suggests that provision of leucodepleted blood components may be as effective as the use of components from CMV-seronegative donors in preventing CMV infection and disease. This is relevant in the UK because Blood Transfusion Services are implementing universal leucodepletion of cellular blood components to minimize the theoretical risk of transmission of new variant Creutzfeldt-Jakob disease. This review examines data on the biology of CMV, discusses options for testing and summarizes the impact of CMV-seronegative and leucodepleted blood components on transfusion-transmitted CMV.

We evaluated whole blood integral filtration to produce leucocyte-depleted red cells and plasma by using the WBF1 whole blood filter (Pall Medsep). Whole blood units were filtered after either warm (2-4 h at room temperature) or cold (12-24 h at 4 degrees C) holds. Filtered and control units were processed using either a bottom-and-top or top-top method. Red cells were tested weekly for 6 weeks, and plasma 3 monthly for 12 months. All filtered red-cell packs contained < 5 x 10(6) leucocytes/unit with 71 of 72 containing < 1 x 10(6) leucocytes/unit. No clinically significant differences in red-cell storage parameters were seen, although haemolysis was less and pO2/pCO2 values were better maintained in filtered units. Plasma units contained < 2.5 x 10(3) leucocytes/unit with no significant loss of factor VIII except in the warm hold units processed by the top-top method. There was no evidence of complement or coagulation activation with significant removal of preformed C3a in cold hold units. Plasma storage parameters were maintained at control levels for 12 months.

Donor leucocytes are responsible for many adverse transfusion effects. Clinical reactions may be attributed to specific leucocyte subsets. In this study leucocyte subpopulations were identified and quantified pre- and post-leucodepletion by integral filtration using novel Optipac(R) configurations incorporating either WBF-1 (Pall Medsep) or RS2000 (Asahi) whole blood filters. Leucocytes were analysed by flow cytometry using direct, four-colour, membrane immunofluorescence with monoclonal antibodies specific for CD 3, 14, 16, 19 and 45. Filtration reduced the leucocyte load by 3-4 log10, consistently giving products with < 2 cells microL-1. Subset distributions were also affected with the proportion of neutrophils and monocytes increased and the lymphocyte/monocyte ratio inverted. These effects were independent of the preprocessing hold conditions, filter used and buffy coat (BC) removal. All filtered red cell products contained 75-80% neutrophils, 16-20% monocytes and 2-7% lymphocytes. Results presented here demonstrate that whole blood filtration, and BC removal, significantly reduce the content and substantially alter the subpopulation distribution of the donor leucocytes remaining in leucodepleted red cell products.

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Progesterone is the only steroid hormone that is essential for the establishment and maintenance of pregnancy in all mammalian species that have been studied. Mice lacking the progesterone receptor (PR) by targeted mutagenesis exhibit abnormalities in all aspects of reproduction including sexual behavior, mammary gland development, ovulation, and implantation. Implantation in PR null mice fails, in part, because the uterine stromal cells cannot undergo differentiation (the decidual cell reaction). Uterine stromal cells do not divide without progesterone and proliferation is blocked by progesterone antibodies and PR antagonism. In spite of the preeminence of progesterone in female reproduction, its molecular mechanisms of action on target cell proliferation and differentiation are not well understood. Recent studies suggest that progesterone plays a direct role in regulating cell cycle transit by increasing the expression and activation of cell cycle regulatory complexes. Furthermore, this progesterone-dependent regulation of cell cycle transit may provide a unique window of opportunity for uterine stromal cells to exit the proliferative cycle, and if exposed to appropriate agents, enter into the differentiation pathway.