HIV AND AIDS (Medical Perspectives Series) by K.E. Nye;J. M. Parkin

By K.E. Nye;J. M. Parkin

A complete account of HIV and AIDS, the administration of the affliction and capability vaccines. This ebook is key studying for scientific scholars and clinicians, and of significant curiosity to scholars and researchers within the lifestyles sciences.

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By K.E. Nye;J. M. Parkin

A complete account of HIV and AIDS, the administration of the affliction and capability vaccines. This ebook is key studying for scientific scholars and clinicians, and of significant curiosity to scholars and researchers within the lifestyles sciences.

Show description

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Extra info for HIV AND AIDS (Medical Perspectives Series)

Sample text

This involves predominantly the IgG and IgA isotypes in adults. This is a result of polyclonal B-cell activation and the antibody produced is mainly to previously encountered antigens. 4 B-lymphocyte dysfunction B-cells in HIV-infected patients are of interest as, despite never having been shown to be infected by HIV in vivo, their function is highly abnormal. 6) and IgM in infants and increased spontaneous Ig production by B-cells in vitro. e. ‘old immunizations’). However, these overactivated cells are unable to respond to new antigens, and are functionally hypogammaglobulinemic.

Difficult to detect in the peripheral blood. Indeed, the studies show a substantial reservoir of virus in the lymph glands of infected individuals which may explain this enigma. 2 Cytokine-mediated depletion HIV infection induces a state of immune activation, with increased production of TNFα and TNFβ, granulocyte-macrophage colonystimulating factor (GM-CSF), IL-1, IL-3, IL-4 and IL-6. 3: Immunopathogenesis of HIV infection. 4: C8166 lymphoblastoid cells are highly fusogenic during HIV infection.

Binding of antigens or mitogens to the T-cell-receptor-CD3 complex and the CD28 cell surface molecule affects gene expression within the cell. g. NF-κB from IκB; the active NF-κB then travels into the nucleus where it binds to other proteins and, in the case of the HIV-infected cell, it binds to the HIV-LTR and can upregulate viral replication). It appears that in the case of gp120 or gp160 binding to the CD4 molecule the signaling pathway is perturbed in such a way that the cell becomes chronically activated and is refractory to further stimulation.

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