Sequence specificity in the higher-order interaction of the Rev protein of HIV-1 with its target sequence, the RRE

Article Abstract:

The HIV-1 protein Rev binds to its target RNA sequence, RRE, and forms larger Rev/RRE complexes by recognizing information in specific RNA sequences. The formation of the Rev/RRE complex plays a crucial role in HIV replication. Researchers tested the ability of Rev to bind to different mutations of RRE that changed the nucleic acid sequence but not the three-dimensional, folding structure of RRE. Different mutations affected the formation of Rev/RRE complexes at different points. For example, some mutations inhibited the initial Rev binding but actually promoted the formation of larger Rev/RRE complexes. Other mutations promoted initial Rev binding but inhibited larger complex formation. These results suggest that all steps of the Rev/RRE complex formation depend upon sequence-specific information, but the initial binding is most dependent upon sequence-specific information.

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An autocrine loop of HIV type-1 Tat protein responsible for the improved survival/proliferation capacity of permanently Tat-transfected cells and required for optimal HIV-1 LTR transactivating activity

Article Abstract:

The HIV-1 Tat protein is involved in a self-regulatory loop which partially protects cells with the tat gene from dying and promotes HIV transcription. Researchers permanently inserted HIV-1 tat genes into a variety of cells and inserted mock genes into control cells. When serum was removed from the culture to cause cell death, the tat-containing cells were partially protected but the control cells were not. However, when antibodies to Tat protein were added to the medium, the tat-containing cells died at the same rate as the control cells. In a similar fashion, tat genes promoted cell proliferation and HIV-1 transcription but these promotional effects disappeared when antibodies to Tat protein were added to the cell cultures. These cells produce a Tat protein that is released and then acts on the same cell to protect it and promote its growth.

Autocrine mechanisms

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Polyamine pools in HIV-infected cells

Article Abstract:

Inhibiting the synthesis of polyamines in HIV-infected cells may not be an effective treatment for HIV infection. Polyamines are natural proteins that occur in most cells and appear to be involved in gene expression. Researchers infected a T-cell line with HIV and measured the levels of the polyamines putrescine, spermine, and spermidine in the culture. HIV did not cause elevated polyamine levels as some other viruses do. Blocking the synthesis of the polamines did not affect the infective ability of HIV.

Infection, Measurement, Lymphocytes, Polyamines

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