In vivo role of IL-6 on the viral load and on immunological abnormalities of HIV-infected patients

Article Abstract:

Increased levels of interleukin (IL)-6 in HIV-infected people may not increase HIV multiplication, but may lead to weakened immune response and metabolic problems. Researchers studied the effects of 21 days of treatment with anti-IL-6 antibody on 11 people with advanced HIV disease. The antibody did not have a significant effect on the amount of virus in the blood, as indicated by measurements of viral antigens, viral RNA, and the virus itself. The antibody also did not affect the abnormally low levels of CD4 and CD19 cells or abnormal levels of chemicals involved in the activation of CD8 cells. Antibody treatment reduced abnormally high levels of C-reactive protein and fibrinogen to a normal level, but did not significantly affect abnormally low albumin levels. The antibody decreased the high levels of B cell activity, which was indicated by a drop in elevated concentrations of immunoglobulins G and A.

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IL-6 induces target cell resistance to HIV-specific cytotoxic lysis

Article Abstract:

Peripheral blood B cells from HIV-positive people appear to produce interleukin-6 (IL-6), a cytokine that can modulate immune responses. IL-6 may induce resistance of target B cells to HIV-specific lysis by cytotoxic T lymphocytes. Transformed B lymphoblastoid cell lines (B-LCL) from six HIV-positive subjects who had not progressed to AIDS were pretreated with exogenous human recombinant IL-6. A reduction in cytotoxic T lymphocytes (CTL) activity was measured in pretreated cells. The HIV-positive subjects produced a mean B-LCL level of 25.2 U/ml, compared to a mean level of 12.7 U/ml for the 14 control subjects. Overproduction of IL-6 in HIV-infected people may allow some disease cells to escape the body's immune system and contribute to the formation of malignant tumors which are seen in AIDS.

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Conservation of total T-cell counts during HIV infection: alternative hypotheses and implications

Article Abstract:

The apparent decline in CD4+ T-type white blood cell levels in patients with HIV infection may reflect a redistribution of T-cells in the body, rather than an absolute reduction. While CD4+ T-cell levels decline in the blood, CD8+ T-cell levels increase, resulting in a relative constancy of the number of T-cells. Researchers evaluate the hypothesis of blind homeostasis, which proposes that the T-cell level remains constant, but the ratio of cell types fluctuates randomly. Redistribution of T-cells between the tissues and the blood may better explain the changes in T-cell ratios seen in HIV infection.

Homeostasis

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