AIDS pathogenesis: from models to viral dynamics in patients

Article Abstract:

Immune functions regenerate cells after HIV infection only up to a point, explaining the gradual progression to AIDS. The delay from HIV infection to the symptomatic stage of AIDS may take as long as 10 years. Researchers point out the early regulatory functions of the immune system, limiting viral replication until a certain threshold is reached. When the number of different viral mutants becomes too large, downregulation fails to operate, causing AIDS symptoms and eventual decline. Free virus in plasma is restored daily, at a turnover of 30%. Rather than boosting the CD4 count, interrupting viral replication may reverse immune deficiency in HIV disease. Initially CD4 cell counts are restored vigorously to almost pre-infection levels, controlling the virus for years. Patients apparently can generate large numbers of CD4 cells even in advanced disease, although the exact nature of this mechanism remains unknown.

AIDS (Disease), Cytopathology, CD4 lymphocytes

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Soluble tumor necrosis factor receptors inhibit phorbol myristate acetate and cytokine-induced HIV-1 expression chronically infected U1 cells

Article Abstract:

A soluble form of the receptor for tumor necrosis factor (TNF) or the TNF-binding protein may inhibit the activation of HIV in HIV-infected cells. Researchers used recombinant forms of soluble TNF receptor (TNFR) and the TNF-binding protein (TBP) in an HIV-infected cell line to determine their effect on HIV activation. Phorbol myristate acetate (PMA) normally activates HIV in cells lines by stimulating TNF synthesis, which ultimately activates HIV replication. TBP and TNFR inhibited the PMA-induced production of p24 antigen in the cell line by 88%. Both compounds reduced HIV activation by PMA even when they were added up to 20 hours after PMA stimulation. TPB also inhibited HIV activation by phytohemagglutinin (PHA), GM-CSF and interleukin 6. TNFR inhibited HIV activation by PHA, GM-CSF and TNF alpha. Recombinant forms of TNFR and TBP could be used to suppress HIV activity in people with HIV infection.

Research, Cell receptors, Tumor necrosis factor

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Human immunodeficiency virus infection abolishes CD4-dependent activation of ZAP-70 by inhibition of p56(super)lck

Article Abstract:

HIV may damage the human immune system in part by inhibiting an enzyme called tyrosine kinase that plays an important role in activating T cells. The enzyme, which is called p56(super)lck, attaches to the CD4 receptor on T cells and phosphorylates other proteins that lead ultimately to T cell activation. In a cell culture of human T lymphocytes that had been infected with HIV, this phosphorylation process was found to be inhibited. The p56(super)lck enzyme also did not bind as well to the CD4 receptor. This could account for the immunosuppression seen in HIV infection.

Phosphorylation

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