Human immunodeficiency virus isolates were studied with respect to syncytium-inducing capacity, replicative properties, and host range. Five of 10 isolates from patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex were able to induce syncytia in cultures of peripheral blood mononuclear cells (MNC). In contrast, only 2 of 12 isolates from asymptomatic individuals had syncytium-inducing capacity. Syncytium-induciiig isolates were reproducibly obtained from the same MNC sample in over 90% of the cases, independent of the donor MNC used for propagation. Syncytium-inducing capacity was shown to be a stable property of an isolate, independent of viral replication rates. Evidence was obtained that the high replication rate of syncytium-inducing isolates observed during primary isolation may be due to higher infectivity of these isolates. The finding that only syncytium-inducing isolates could be transmitted to the H9 cell line is compatible with this higher infectivity. The frequent isolation of syncytium-inducing isolates from individuals with AIDS-related complex or AIDS and the apparent higher in vitro infectivity of these isolates suggest that syncytium-inducing isolates may unfavorably influence the course of human immunodeficiency virus infection.

To investigate the effect of persistent HIV infection on the immune system, we studied leukocyte functions in 14 asymptomatic homosexual men (CDC group Il/III) who were at least two years seropositive, but who still had normal numbers of circulating Cfl4+ T cells. Compared with age-matched heterosexual men and HIV-negative homosexual men, the CD4' and CD8' T cells from seropositive men showed decreased proliferation to anti-CD3 monoclohal antibody and decreased CD4' T-helper activity on PWM-driven differentiation of normal donor B cells. Monocytes of HIV-infected homosexual men showed decreased accessory function on normal T cell proliferation induced by CD3 monoclonal antibody. The most striking defect in leukocyte functional activities was observed in the B cells of HIV-infected men.

Petunia hybrida mutants, homozygous recessive for one of the genes An1, An2, An6, or An9 do not show anthocyanin synthesis in in vitro complementation experiments per se (see also Kho et al. 1977). Extracts of flowers of these mutants all provoke anthocyanin synthesis in isolated petals of an an3an3 mutant. Mutants homozygous recessive for one of the genes An1, An2, An6, or An9 and homozygous recessive for F1 accumulate dihydroflavonols in comparable amounts. The synthesis of dihydromyricetin is blocked in an1an1 mutants, which indicates a regulating effect of the gene An1 on the gene Hfl. Similar mutants, but dominant for F1, accumulate flavonols (kaempferol and quercetin) instead of dihydroflavonols. Myricetin is accumulated in minor amounts and not at all in an1an1 mutant. Furthermore, the synthesis of this flavonol is not controlled by the gene F1. The synthesis of cyanidin (derivatives) is greatly reduced when flavonols are synthesized (F1 dominant). In mutants dominant for Ht1 and Hf1 and thus able to synthesize cyanidin (derivatives) and delphinidin (derivatives), predominantly delphinidin (derivatives) are synthesized. The results indicate that kaempferol (derivatives), quercetin (derivatives), and delphinidin (derivatives) are the main endproducts of flavonoid biosynthesis in Petunia hybrida.

The early effects of infection with human immunodeficiency virus (HIV) were investigated in homosexual men who had seroconverted for anti-HIV antibodies. Leukocyte functional activities were determined in longitudinally collected peripheral blood mononuclear cell samples. During the first 10 months following seroconversion, anti-CD3 monoclonal antibody-induced T cell proliferation, monocyte accessory function and T helper activity on B cell differentiation in a pokeweed mitogen-driven system were not affected. In contrast, from the moment of seroconversion on, B cells of seroconverted men failed to produce immunoglobulin in the pokeweed mitogen-driven system. This defect was not restored by addition of normal CD4+ T cells. Immunoglobulin synthesis induced by Staphylococcus aureus and interleukin 2 decreased gradually, until it was completely lost 10 months after seroconversion. In addition, proliferation in response to anti-IgM or Staphylococcus aureus by B cells from HIV seroconverted men was decreased. The lack of inducible in vitro B cell activity was not accompanied by elevated spontaneous Ig synthesis by B cells of the seroconverted men. In the second group of men studied during the 2nd year following seroconversion, T helper activity on normal B cell differentiation significantly decreased, whereas anti-CD3-induced T cell proliferation and monocyte accessory function were not significantly affected. Our results demonstrate that in almost all HIV-infected individuals B cell functional defects are the first leukocyte abnormalities observed preceding defects in T helper activity.