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Here we present a numerical study of a nonlinear model of HIV dynamics. The model describes the dynamics of T4 lymphocytes cells, HIV virus and opportunistic infection, and includes the effect of HIV treatment. We show that, as the efficacy of the antiretroviral treatment is reduced, the model display a transition from orderly to chaotic dynamics via a period-doubling cascade. The chaotic regime is interrupted by regions of periodic dynamics known as periodic windows.

We discuss how chaotic dynamics can develop in a recently proposed model of the interaction between the human immunodeficiency virus HIV and the human immune system. The model describes the state and number of T4 lymphocytes as they interact with HIV and with a secondary infectious agent.

Substituted Schiff bases of l-amino-3-hydroxyguanidine (SB-HAG) were tested for the first time against noninfected T4 lymphocytes (CEM-6 cells) and the same cell line infected by HIV-1 in vitro. Twenty-one of 23 compounds at micromolar levels did not inhibit the growth of the noninfected T4 cells, suggesting minimal cytotoxicity. The antiviral effects of these compounds in a micromolar concentration range have been shown to be nonsignificant (

Forty-five Swedish chimney sweeps and 49 controls were investigated with micronuclei stimulated by phytohemagglutinin and pokeweed mitogen and by analysis of lymphocyte subgroups and neutrophilic leukocytes. There was a statistically significant effect among sweeps with respect to both micronuclei variables and neutrophilic leukocytes. The effect on lymphocyte micronuclei was most prominent in pokeweed mitogen-stimulated cells, which may imply that the T4 lymphocytes were preferentially damaged by the occupational exposure.

The publication, in 1981, of a report announcing the occurrence of a cluster of diagnoses of a rare form of pneumonia due to the microorganism Pneumocystis carinii in a group of male homosexuals in San Francisco constitutes the first notice of the advent of a new disease. It was quickly recognized, subsequent to that report, that the occurrence of this then rare infection was secondary to the profound depletion of the immune system caused by the new disease, which soon acquired the name of Acquired Immune Deficiency Syndrome, or more familiarly, AIDS. The causative organism was identified as a retrovirus, named Human Immunodeficiency Virus (HIV), which attacks the T4 lymphocytes of the immune system.

SUMMARY Trimethoprim-sulfamethoxazole and parenteral pentamidine isethionate are effective in 60 to 80 per cent of AIDS patients with pneumocystis pneumonia. Adverse reactions are frequent with both agents, but because the adverse reactions are less severe with trimethoprim-sulfamethoxazole, this agent is the drug of choice for patients who are not known to be intolerant of it. The recommended duration of therapy is 21 days. Aerosolized pentamidine and intravenous trimetrexate are investigational agents that show considerable promise, but their role in the therapy of pneumocystis pneumonia will have to be demonstrated in controlled trials. For patients who fail to respond to conventional agents after 5 to 10 days of therapy, therapeutic alternatives to consider would be trimetrexate, DFMO, or high-dose corticosteroids, the latter given with conventional agents. Prophylaxis against pneumocystis pneumonia is appropriate for HIV- infected patients with fewer than 300 T4 lymphocytes per cu mm, even if they are receiving zidovudine (Retrovir). It also should be considered in patients with a prior history of this infection, irrespective of the T4 count. The efficacy of trimethoprim-sulfamethoxazole, pyrimethamine-sulfadoxine, or aerosolized pentamidine has not yet been substantiated. Many patients cannot tolerate the first two combinations chronically.

The subpopulations of T lymphocytes, B lymphocytes and macrophages of the peripheral blood in 58 cases of epilepsia were studied with McAb by IFA method. The activity of natural killer (NK) cells of peripheric blood monocyte was investigated by 51Cr-releasing method. 22 healthy donors of about the same age served as controls. The results showed that the percentage of T3 and T4 lymphocytes in epileptic patients was decreased, and the ratio of T4/T8 was markedly reduced as compared to control group. The percentage of T8 lymphocytes was increased. There were no significant changes in B lymphocytes and macrophages. The NK cell activity also showed decrease. The results suggested abnormality in cellular immunity in epilepsia, which may be involved in the pathogenetic mechanism of the disease.

Previously the authors demonstrated that most patients with AIDS have serum antilymphocyte antibodies. Therefore, in an attempt to decrease these antibodies and at least transiently increase blood lymphocytes, they treated one AIDS patient with three courses of plasmapheresis. During or after each course, his T4 lymphocytes rose significantly but subsequently fell to baseline values within two weeks after therapy. The increase in T4 lymphocytes was associated with removal of patient plasma rather than infusion of heterologous plasma. These results suggest the need for more investigation into plasmapheresis as adjunct therapy for AIDS.

While B lymphocytes can bind antigen directly, T lymphocytes recognize antigen only when presented together with major histocompatibility complex (MHC)-en-coded class I or II molecules in the membrane of antigen-presenting cells (APC). This is called MHC restriction and was first shown in animal studies (see [5, 25] for references). The parts of the MHC molecule which are co-recognized together with antigen are often called restriction elements.

SUMMARY We measured the number of Langerhans cells in clinically normal epidermis and the number of T4 lymphocytes in the plasma in 24 patients infected with HIV, and related these to the stage of the disease. A correlation is demonstrated between the numbers of Langerhans cells and T4 lymphocytes. Numbers of Langerhans cells were lower in patients with disease stages III and IV than in those with disease stage II. Thus Langerhans cell numbers could be of prognostic value in this disease.

Several mathematical models describing the interaction of HIV with T4 lymphocytes and macrophages are presented. The primary problems addressed involve the decline of immunocompetence as mirrored by the T4 cell number, the role of macrophages in the disease process, the interaction in early stages of AIDS, and the fraction of infected circulating T4 cells.