Protection of a T-cell line from human immunodeficiency virus replication by the stable expression of a short antisense RNA sequence carried by a shuttle RNA molecule

Article Abstract:

A gene carried by certain viruses, known as the VA1 gene, may be modified prevent the multiplication of the HIV-1 virus in T cells. Researchers used the polymerase chain reaction to generate VA1-c-rev RNA with a small antisense section that matched a section of HIV-1 DNA and a VA1-C-rev RNA with an uncomlimentary section. Both types of RNA were inserted into the CEM line of T cells which were then grown in culture. Northern blot and gel electrophoresis were used to establish the presence of the RNA in the cells. The cells were then infected with HIV-1 and HIV-2, which are genetically different. HIV-1 multiplied in the cells with random RNA but not in the cells with VA1-c-rev RNA, even 90 days after infection. HIV-2 multiplied in both types of cells. Thus, VA1-C-rev RNA specifically blocked the replication of HIV-1.

Usage, Gene therapy, Antisense RNA, Virus inactivation

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Induction by human immunodeficiency viruses types 1 and 2 of degradation of CD4 but not of a CD4 mutant unable to bind viral envelope glycoproteins

Article Abstract:

The binding of the CD4 T cell receptor to a viral glycoprotein appears to be necessary for the reduction in CD4 receptors seen during HIV infection. The CD4 receptor is the area on T cells that HIV binds to in order to infect the cell. Researchers infected T cells in culture with HIV-1 or HIV-2 and measured the number of CD4 receptors while the virus reproduced in the cells. CD4 receptor levels dropped in each case. The drop in CD4 receptor levels during HIV-2 reproduction was unexpected because this viral strain does not contain a protein called vpu that was thought to be involved in this process. In addition, CD4 receptor levels did not drop when the researchers used a cell line that contained a defective form of the CD4 receptor that can not bind to viral glycoprotein.

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T cells chronically infected with HIV do not contain sufficient Nef to promote CD4 downmodulation in the absence of envelope-mediated effects

Article Abstract:

The Nef protein may not be produced in sufficient quantities to affect the regulation of the CD4 receptor. This receptor on T cells is the primary means by which HIV enters the cell. This occurs because the receptor can bind to viral envelope glycoproteins. However, these glycoproteins can also affect the production of the CD4 receptor. Using T cell cultures, researchers found during the late stage of viral reproduction, the Nef protein is not present in sufficient quantities to affect CD4 production. At this stage, viral envelope glycoproteins appear to be the major influence on the CD4 receptor.

Physiological aspects, Viral envelopes, Virus receptors

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