Abstract
In infected cells, HIV replication is regulated at least by three virus encoded proteins. The product of tat gene is a positive transcriptional regulator, the product of rev gene regulates the transport of viral mRNA encoding the structural proteins from the nucleus to the cytoplasm while the products of the nef gene may have a negative regulatory effect. However, the transcriptional activity of the promoter (LTR) can also be stimulated by various extracellular stimuli such as mitogens, cytokines and differentiation factors, or by infection with several heterologous viruses including the herpesviruses that often accompany HIV infection in AIDS patients. The molecular mechanism by which the herpesviruses enhance the transcriptional activity of HIV-LTR is not clear. However, it was shown that activation is mediated by the products of herpesvirus immediate early (IE) genes and probably proceeds through stimulation of cellular transcriptional factors such as NF-кB. The activity of HIV-LTR can be down-regulated by methylation, which is accompanied by the reduced capacity of this region to bind the trans-activating nuclear protein. The stimulation of methylated HIV-LTR expression by HSV-1 infection seems to involve hypomethylation, while tat-mediated trans-activation occurs without an apparent change in LTR methylation.
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Pitha, P.M., Bednarik, D.P. (1990). Trans-Activation of the Human Immunodeficiency Virus (HIV) Promoter by Heterologous Virus Infection. In: Aurelian, L. (eds) Herpesviruses, the Immune System, and AIDS. Developments in Medical Virology, vol 6. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1507-0_12
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DOI: https://doi.org/10.1007/978-1-4613-1507-0_12
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