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Few studies have specifically examined defective provirus in asymptomatic human T-lymphotropic virus Type 1 (HTLV-1) carriers and its relation to proviral DNA loads (PVLs). To assess the significance of defective provirus in asymptomatic carriers, we examined PVLs in peripheral blood mononuclear cells of 208 asymptomatic HTLV-1 carriers. The mean PVLs determined using primers for the pol region were less than that for the pX region in these carriers. Analysis of seven carriers with high PVLs for the pX region but lower PVLs for the pol region showed that four had single nucleotide polymorphisms of proviral genomes for the pol region and three had HTLV-1-infected cells with defective provirus. Three carriers with defective provirus showed high PVLs at their initial screens, and PVLs increased after a 10-to 12-year interval in two carriers. Southern blot assay showed clonal expansion of HTLV-1-infected cells, and the predominant clones changed during the observation period. These data suggest that although HTLV-1-infected cells with defective provirus may have a growth advantage, the predominant clones of HTLV-1-infected cells do not always survive for many years in asymptomatic carriers.

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Intrauterine transfusion is the standard antenatal treatment for a fetus with severe anemia. Plasmapheresis is an alternative treatment for cases with a history of severe hemolytic disease of the fetus and newborns at less than 20 weeks of gestation. There is only one previous report of plasmapheresis for the anti-M alloimmunization in pregnancy, and we report here on the successful treatment of plasmapheresis for anti-M alloimmunization. A woman with a history of intrauterine fetal death at 24 weeks of gestation due to severe fetal anemia caused by anti-M alloimmunization received plasmapheresis once or twice a week from 14 weeks of gestation onward. An intrauterine blood transfusion was conducted at 28 weeks, and a cesarean section was performed at 31 weeks. The infant had anemia and jaundice but was discharged at day 46. Plasmapheresis may delay the development of fetal anemia and reduce the risk of early and repeat intrauterine transfusion in cases of anti-M alloimmunization in pregnancy.

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