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Human immunodeficiency virus type 1 (HIV-1)-infected H9 and blood mononuclear cells (MNCs) were studied by immunogold electron microscopy for the presence of HIV-1 gag p24 protein, env gp41 and gpl20 proteins, and host cell molecules CD4, CDlla, CD25, CD54, CD63, HLA class I and HLA-DR. Uninfected H9 cells and MNC membranes labelled for CD4, HLA class I and class II, and, at low density, CDlla and CD54; lysosomal structures in the cytoplasm labelled for CD63. The infected cell surface showed immunolabelling for HIV-1 proteins, as did budding particle-like structures.Immunogold labelling of the cell membrane for CD4 was almost non-existent. The level of immunolabelling for CD1 la and CD54 on infected cells was greater than that on uninfected cells; this is presumably related to a state of activation during virus synthesis. Budding particle-like structures and free virions in the intercellular space were immunogold-labelled for all host cell markers investigated. This was confirmed by double immunogold labelling using combinations of HIV-1 gag p24 labelling and labelling for the respective host cell molecule. We conclude that virions generated in HIV-1-infected cells concentrate host-derived molecules on their envelope. Also molecules with a prime function in cellular adhesion concentrate on the virion.Infection of cells by human immunodeficiency virus type 1 (HIV-1) is followed by the disappearance of the virus receptor molecule CD4 from the cell membrane (Geleziunas et al., 1991 ;Gielen et al., 1989; Hoxie et al., 1986). This phenomenon has also been observed for other surface molecules including HLA antigens (Eales et al., 1988; Gelderblom et al., 1987b;Henderson et al., 1987;Kerkau et al., 1989;Schols et al., 1992) and the CD3, CD8 and CDll antigens (Stevenson et al., 1987). By using immuno-electron microscopy we have previously demonstrated the complete absence of CD4 antigen and the partial absence of HLA-DR and CD5 antigen on H9 cells 2 days after HIV-1 infection (Meerloo et al., 1992). The CD3 and CD25 antigens remained detectable on the cell surface at similar density, and the CD63 antigen, a t Present address:

Thirty-six 7-mo-old gilts were used to study the effects of dietary vitamin E and fat source (5% sunflower oil or animal fat) in pregnant and lactating sow diets on serum vitamin E concentration and on cell-mediated and humoral immune response in suckling and weaned piglets. Six gilts each received one of six diets throughout pregnancy and lactation. The basal diets (13 mg alpha-tocopherol/kg diet) were supplemented with dl-alpha-tocopheryl acetate to 48 and 136 mg alpha-tocopherol/kg of feed (average analyzed values). After weaning (at 4 wk of age) all pigs received identical diets (20 mg of alpha-tocopherol/kg feed). One week after weaning, pigs were immunized (i.m. with ovalbumin and tetanus toxoid) and antibody production was measured. Blood samples were taken immediately after birth, at 1 wk after birth, at weaning, and at four weekly intervals after weaning. Samples were analyzed for alpha-tocopherol concentration, total number of leukocytes, T- and B-lymphocytes, lymphocyte stimulation with concanavalin A, lysozyme activity, and immunoglobulin concentrations. It was concluded that a high vitamin E level in the sow's diet increased serum vitamin E concentration of 1-wk-old pigs (P less than .05). Immune response against ovalbumin was increased (P less than .05) at 1 wk of age after immunization for weaned pigs from sows fed the high level of vitamin E. Also, the phagocytic measures of pigs at 1 wk of age were increased by the medium vitamin E level (P less than .05). Fat sources in the sow's diet had no consistent effect on the immunological measures of pigs.

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ORIGINAL PAPERS current state of fasting. The correlation coefficients (Table 4) showed that, compared to animals infected with Tvivax, animals infected with Tcongolense with a greatly decreased DMI showed a smaller increase in plasma urea, but a greater increase in plasma NEFA and BHBA. In addition, plasma TP levels were lower in animals Infected with Tcongolense than in animals infected with Various characteristics of the KLH-specific immune response were studied in 988 sows of four breeds. KLHspecific immune responses showed considerable variability. The applied statistical model explained 63 to 73 per cent of this variation. influences, expressed as the heritability estimate, were rather high for the IgG response (0.33), as well as for the skin reaction (0.26) and the LST (0.41 -0.45). A positive correlation between the various immune parameters was found. Selective breeding for immune responsiveness seems to be feasible, but selection for cellular as well as