By Jeffrey Laurence (auth.), Jean-Marie Andrieu, Wei Lu (eds.)
In the prior decade, the worldwide efforts within the keep an eye on of HIV ailment have been primarily focused on the hunt for anti-retroviral brokers. up to now, anti-HIV remedies were proven to be disappointing due to quick improvement of drug-resistant mutant versions. regardless of this hindrance within the healing struggle opposed to HIV an infection, antiviral learn could be actively pursued. although, failure of antiviral remedy exhibits that different avenues of analysis might be speedily explored with an analogous strength. during this environment, extraordinary advances were lately made within the dissection and realizing of the viro-immunological procedures governing the revolutionary destruction of lymphoid organs linked to AIDS enhance ment, and HIV-induced activation and apoptosis were pointed out as key phenomena of the immune process destruction. This ebook assembles the newest advances on uncomplicated and scientific facets ofT-cell activationiapoptosis in HIV an infection and their implications for immunotherapy. those facts have been offered at a world symposium hung on July 11-12, 1994, in Paris. The booklet is partitioned into 21 chapters masking 4 finished fields: 1) T-celllmacrophage activation and HIV an infection; 2) Apoptosis and viropathogenesis of hello V affliction; three) Apop tosis and immunopathogenesis ofHIV disorder; four) Mediators ofT-cell activationiapoptosis and healing functions. we are hoping that this publication will support the readers in realizing contemporary advances within the viro-immunopathogenesis of hello V illness in addition to the rationales for power immune cell-targeted healing interventions.
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Extra info for Cell Activation and Apoptosis in HIV Infection: Implications for Pathogenesis and Therapy
Sample text
26 30 J. Zack Why infection and subsequent depletion of the immature CD4+/CD8+ subset is initially seen in human thymic implants in SCID-hu mice is an intriguing question. Flow cytometric analysis indicates that the level of CD4 on the surface of the immature cells is not appreciably higher than on the more mature popUlation, so virus binding and entry is likely not the mechanism resulting in increased infection at early timepoints. Rather, it is likely that this immature population is the more metabolically active population, which allows for increased viral replication in this subset.
Thus, macrophages appear fully permissive to productive HIV-I replication while non-dividing (GO T cells) restrict virus replication at a step which proceeds nuclear import of viral DNA. The requirement for T cell activation in productive HIV-I replication has important implications for the relationship between immune activation and virus burden. It remains to be determined whether modulating the immune activation status of the infected individual may provide an opportunity for modulating virus burden and influencing disease course.
In agreement with this result, experiments by one of our collaborators (Dr. M. Emerman), using an integration dependent assay (Kimpton and Emerman, 1992) confirmed that under conditions of G2 arrest (gamma irradiation) viral MT4/HIV -AphidicoIjn Tme post·infection (h) 3 5 8 MT4/HIV + AphidicoIin 24 3 5 8 24 MT4/HIV +AZT 3 5 8 24 Pol 2 LTR circle • Figure 2. Kinetics of HIV-I DNA synthesis and nuclear import in proliferating and in G liS arrested CD4+ T cells. MT 4 cell cultures were growth arrested by the action of aphidicolin.
