Titlebook: Cell Activation and Apoptosis in HIV Infection; Implications for Pat Jean-Marie Andrieu,Wei Lu Book 1995 The Editor(s) (if applicable) and

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Rational Problems Associated with the Development of Cellular Approaches in Controlling HIV Spread, was proposed even before HIV was implicated as a cause of AIDS, mainstream research has been oriented toward goals that were easier to grasp. As a result, little progress has been made to adopt the viral ‘kamikaze’ phenomenon to the development of a meaningful therapeutic strategy.

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Mechanism of Apoptosis in Peripheral Blood Mononuclear Cells Of HIV-Infected Patients,y flow cytometry. CD4XL was found to result in increased Fas expression as well as Fas mRNA in lymphocytes and the up-regulated Fas Ag was closely correlated with apoptotic cell death. CD4XL in PBMC also resulted in induction of the cytokines INF-τ and TNF-α in the absence of IL-2 and IL-4 secretion

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Programmed Death of T Cells in the Course of HIV Infection,gulation of the Thl/Th2 cytokine balance (reviewed in (.)). Following the hypothesis by Ameisen et al (.), who proposed apoptosis as a mechanism for CD4+ T-cell depletion and loss of cellular immune function, several groups, including our group, have investigated PCD of (CD4+) T cells as a possible

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Patty Joldersma,Koos van Nugteren cell lineage may not represent true molecular latency, with absent expression of viral transcripts and protein. Yet latency and viral persistence both involve two essential elements: initial restriction at the level of proviral transcription or initiation, regulated at HIV’s long terminal repeat (L

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Patty Joldersma,Koos van Nugterention (82%) showing abnormally high levels of these than abnormally low levels of CD4 (52%; p<0.001). Examining activation of the CD4 subset specifically is likely to be of greater interest, given that this cell is the viral target. Indeed, we found that in the cross-sectional study, levels of HLA-DR

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Behandelen van een persoon met oedeem,ound that agents that arrest the cell in the late G. phase of the cell cycle do not alter the ability of the virus to complete reverse transcription. However, agents that inhibit activation of the cell by blocking transition through G. prevent completion of reverse transcription. It thus appears tha

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