Prevention of HIV-1 infection and preservation of CD4 function by the binding of CPFs to gp120

Article Abstract:

CD4, a cell-surface receptor for class II major histocompatibility antigens, has achieved notoriety by also being the primary receptor for the AIDS virus, HIV. Several major experimental therapeutic protocols hinge upon trying to interfere with the binding of the virus to CD4, the first step in the infectious process. While most such experiments focus upon the use of antibodies to block CD4, or using an excess of recombinant CD4 to swamp the virus, researchers have now identified a set of organic compounds which block the binding of the virus. The molecules are N-carbomethoxycarbonyl-prolyl-phenylalanyl benzyl esters, more simply called CPFs. These molecules bind to gp120, which is the viral molecule responsible for binding to the receptors on the target cell. One particular CPF, termed CPF(DD) was found to block viral binding without interfering with the normal function of the T cell. In tissue culture experiments, CPF(DD) was shown to prevent the spread of infection from cell to cell. However, the production of viral proteins by cells which have already been infected by the AIDS virus is not affected by this compound. In principle, however, the binding of CPFs to the viral protein could be exploited to deliver other reagents specifically to infected cells while leaving uninfected cells alone. The ability of CPFs to bind to gp120 indicates that these agents have considerable therapeutic potential for the treatment of HIV infection. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects, Cell receptors, AIDS (Disease), gp120 (Medication)

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Selective elimination of HIV-1-infected cells with an interleukin-2 receptor-specific cytotoxin

Article Abstract:

Experiments were carried out to evaluate the effectiveness of one approach to preventing infection by human immunodeficiency virus type 1 (HIV-1), which is associated with AIDS. This virus binds to the CD4 receptor, a molecule on T cells, causing them to be activated. (T cells are the main cell type of the cellular immune system.) One of the signs of this activation is the expression of the receptor for interleukin-2 (the IL-2 receptor); when this occurs, HIV-1 begins to replicate and infection proceeds. In these experiments, a toxin (diphtheria toxin) was joined to IL-2 to produce a molecule (DAB IL-2) that would bind to the IL-2 receptor and kill the cells on which the receptor was expressed. T cells were infected with HIV-1 under laboratory conditions, then exposed to DAB-IL2. This led to the elimination of the infected cells, while uninfected T cells were not eliminated. Other tests of the selectivity of this effect for infected cells were carried out. In addition, the toxin prevented HIV-1 from producing certain proteins and new infectious viral particles. The use of targeted toxins, such as that described here, may be effective in curbing the initial spread of HIV infection. (Consumer Summary produced by Reliance Medical Information, Inc.)

HIV (Viruses), HIV, Interleukin-2, Drug receptors

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PIK-related kinases: DNA repair, recombination, and cell cycle checkpoints

Article Abstract:

A new kinase family has been cloned that participates in a variety of cellular functions including meiotic and V(D)J recombination, cell cycle progression and chromosome maintenance and repair. When functioning improperly, the new kinase family can cause cancer and other disorders.

Research, Cellular control mechanisms, Cell regulation, Protein kinases

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