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Updated: Aug 10, 2026

An In Vitro Model for Measuring Immune Responses to Malaria in the Context of HIV Co-infection
Published on: October 6, 2015
[Impairment of the immune system by HIV infection]
CD4 + T-helper lymphocytes are the main target cells in HIV infection. Since CD4 molecules are not restricted to T-cells but also found on monocytes, macrophages, follicular dendritic cells, Langerhans cells, and microglial brain cells, these cells might be affected, too, by HIV. HIV binds via the gp 120 envelope protein to the 67 KD CD4 membrane protein. Patients with HIV infection show distinct autoimmunological reactions against the cells of their immune system. Autoantibodies directed against CD4 cells seem to be responsible for the extent of the immune deficiency and are, therefore, of prognostic value. Aside from CD4+ cell depletion, the functional impairment of the T-cell system plays an important part in the progress of the disease. Patients with depressed gamma-interferon production after stimulation with antigens are at a risk for AIDS-related opportunistic infections. Polyclonal production of immunoglobulins and impaired stimulation of B-cells are characteristic for B-cell dysfunction. NK-cell dysfunction depends on reduced production of IL-2 and altered gamma-interferon production of T-cells infected with HIV.
CD4 + T-helper lymphocytes are the main target cells in HIV infection. Since CD4 molecules are not restricted to T-cells but also found on monocytes, macrophages, follicular dendritic cells, Langerhans cells, and microglial brain cells, these cells might be affected, too, by HIV. HIV binds via the gp 120 envelope protein to the 67 KD CD4 membrane protein. Patients with HIV infection show distinct autoimmunological reactions against the cells of their immune system. Autoantibodies directed against CD4 cells seem to be responsible for the extent of the immune deficiency and are, therefore, of prognostic value. Aside from CD4+ cell depletion, the functional impairment of the T-cell system plays an important part in the progress of the disease. Patients with depressed gamma-interferon production after stimulation with antigens are at a risk for AIDS-related opportunistic infections. Polyclonal production of immunoglobulins and impaired stimulation of B-cells are characteristic for B-cell dysfunction. NK-cell dysfunction depends on reduced production of IL-2 and altered gamma-interferon production of T-cells infected with HIV.
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