Download AIDS Vaccine Research by Flossie Wong-Staal, Robert C. Gallo PDF

By Flossie Wong-Staal, Robert C. Gallo

This reference describes the most recent advances within the improvement and layout of an HIV preventive vaccine-detailing the pathogenesis and genetic variability of HIV an infection for the development of molecular and healing concepts to lessen the development and transmission of AIDS. With contributions via universally well-known experts within the box, AIDS Vaccine study discusses

  • major stumbling blocks within the identity of a preventive vaccine
  • the position of innate immunity in administration of HIV an infection
  • the influence of hugely energetic antiretroviral remedy (HAART) on AIDS examine
  • the construction of a good mucosal DNA vaccine
  • the influence of the AIDS epidemic on constructing nations delivering approximately 2000 modern references to facilitate additional examine, AIDS Vaccine study is a well timed guide compatible for immunologists, virologists, pathologists, epidemiologists, pharmacologists, microbiologists, hematologists, hepatologists, AIDS researchers, and upper-level undergraduate and graduate scholars in those disciplines.
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    Sample text

    The proximate cause of the susceptibility to opportunistic infections observed with advancing disease is the defects in T-cell number and function that result directly or indirectly from HIV infection. , the major costimulatory receptor that is necessary for normal activation of T cells) is reduced during HIV infection compared to cells from uninfected individuals (365). CD28Ϫ cells do not respond to activation signals and express markers of terminal activation, including HLA-DR, CD38, and CD45RO (366).

    This transition may occur by mutation of only a few amino acid residues predominantly in the envelope V3 loop (116,117,122,123). Given the high error rate of RT and the rapid kinetics of HIV replication, the surprising failure of such mutants to emerge until late in the course of the disease process indicates a change in the selective advantage of such a mutation during the course of disease progression. The nature of such a selective advantage is currently unknown; however, it may relate to the ability of X4 viruses to gain cellular entry through an expanded repertoire of coreceptor molecules.

    In nonhuman primate models, neutralizing antibodies are associated with slow rates of disease progression (195) and accelerate clearance of both infectious and noninfectious virions (196); furthermore, passive transfer of SHIV-neutralizing antibodies can protect macaques against a subsequent viral challenge (197–200). Some anti-HIV antibodies bind to IgG Fc receptor-positive cells and sensitize them to mediate antibody-dependent cellular cytotoxicity (ADCC) against HIVinfected or HIV-coated cells (201,202).

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