An analysis of the mechanisms involved in HIV infection and the role of chemokines in suppression of HIV replication.
Written in 2008; 2,060 words; 8 sources; MLA; $ 64.95
Paper Summary:
This paper analyzes the relationship between immunobiology and HIV. It analyzes the research in an attempt to understand the mechanisms involved in HIV infection and in the operation of various related biological effects. The paper then addresses the role of the chemokine MIP-1 beta, among others, in T cell mediated suppression of HIV replication.
From the Paper:
"Patke, Green, and Shearer examine the role of beta-chemokines and their chemokine receptor on HIV B lymphocyte function. To test this interaction, the researchers used highly purified normal human B cells from seronegative donors, isolating them by adherence to CD19-coated beads. They then treated IL-4 plus anti-CD40-activated B cells with recombinant gp120 (10 ng/ml) before exposure to beta chemokines or receptor. At that stage, cyclic nucleotide generation was assessed at six hr, DNA synthesis at day threem and IgM production on day seven. Also, cell surface marker expression was determined by flow cytometric analysis using the Coulter EPICS-XL. What the researchers found was that there ia a role for MIP-1 beta and RANTES on the early B cell events of proliferation, cyclic nucleotide generation, and cell surface marker receptor modulation in opposition to the beta chemokine receptor, CCR5. the researchers also note that the ability to regulate early B cell events might be a targeted area in the development of novel designer molecule therapeutic approaches to AIDS, though further research is needed finally to demonstrate this possibility."
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