Antibodies against defined carbohydrate structures of Candida albicans protect H9 cells against infection with human immunodeficiency virus-1 in vitro

Article Abstract:

Candida albicans is a yeast that causes infections commonly seen in patients whose immune systems are not functioning properly. The infection is seen in most patients with AIDS and in many people who are infected with HIV, the human immunodeficiency virus. There are two types of C. albicans - type A and type B - and both are found in immunosuppressed patients. The antibodies produced to C. albicans by the immune system may also inhibit the action of HIV. In a study using New Zealand rabbits, antibodies to C. albicans and HIV gp120 were raised, and their effectiveness against HIV was measured, as was their effect on uninfected cells (gp120 is a glycoprotein of HIV). Anti-Candid antibodies were found to be effective inhibitors of HIV replication in cells, optimally at four days after infection. There was strong evidence that the antibodies could recognize gp120 of HIV, but the results do not provide direct evidence that the antibodies interfere with the gp120-CD4 binding, thought to be the mode of transmission of HIV infection. Antibodies to type A C. albicans better neutralized the activity of HIV than antibodies to type B C. albicans, but the significance of this is not known. The antibodies also showed no effect on non-HIV-infected cells. This is important information for the development of antiviral therapy and vaccines against HIV infection. (Consumer Summary produced by Reliance Medical Information, Inc.)

Research, Candidiasis, AIDS vaccines, Candida albicans, Antibodies

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HIV-1 gp120 and NMDA induce protein kinase C translocation differentially in rat primary neuronal cultures

Article Abstract:

HIV-1 glycoprotein 120 (gp120) appears to significantly elevate levels of intracellular calcium ions and induce greater translocation of protein kinase C (PKC) from inside the cell to the cell membrane than N-methyl D-aspartate (NMDA). Rat cells die after exposure to HIV-1 gp 120, and it is thought that the cell death results from gp120's indirect effect on NMDA receptors. In cultures of rat cells, both gp120 and NMDA induced PKC translocation. gp120 caused a significant rise in intracellular calcium ions. Treating cells with compounds that block NMDA receptor channels completely prevented PKC translocation induced by NMDA and reduced PKC translocation induced by gp120. The viability of cells before treatment with gp120 was 84.8% compared with 28.7% after treatment with gp120. Treating cells exposed to gp120 with the compounds that block NMDA receptors restored their viability. gp120 appears to cause cell death by sensitizing the NMDA receptors.

Causes of, Cell death, Protein kinases, HIV antigens

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Expression of nuclear lectin carbohydrate-binding protein 35 in human immunodeficiency virus type 1-infected Molt-3 cells

Article Abstract:

Expression of the nuclear carbohydrate-binding protein 35 (CBP35) appears to increase with the onset of the tat gene expression, which regulates viral replication, and decreases afterwards. Researchers analyzed the alternation of CBP35 messenger-RNA of HIV-1 infected and uninfected Molt cells using Northern blot analysis. Over a five-day period beginning with the initial infection of the cells, RNA-blot hybridization was performed to measure the level of CBP35 messenger RNA expression and of tat messenger RNA expression. CBP35 expression peaked at day 2 and declined linearly thereafter. Tat messenger RNA began to rise during the second day and increased thereafter.

HIV infection, HIV infections

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