Balance between retroviral latency and transcription : based on HIV model
The representative of the Lentivirus genus is the human immunodeficiency virus type 1 (HIV-1), the causative agent of acquired immunodeficiency syndrome (AIDS). To date, there is no cure for AIDS because of the existence of the HIV-1 reservoir. HIV-1 infection can persist for decades despite effective antiretroviral therapy (ART), due to the persistence of infectious latent viruses in long-lived resting memory CD4+ T cells, macrophages, monocytes, microglial cells, and other cell types. However, the biology of HIV-1 latency remains incompletely understood. Retroviral long terminal repeat region (LTR) plays an indispensable role in controlling viral gene expression. Regulation of the transcription initiation plays a crucial role in establishing and maintaining a retrovirus latency. Whether and how retroviruses establish latency and reactivate remains unclear. In this article, we describe what is known about the regulation of LTR-driven transcription in HIV-1, that is, the cis-elements present in the LTR, the role of LTR transcription factor binding sites in LTR-driven transcription, the role of HIV-1-encoded transactivator protein, hormonal effects on virus transcription, impact of LTR variability on transcription, and epigenetic control of retrovirus LTR. Finally, we focus on a novel clustered regularly interspaced short palindromic repeats-associated protein 9 (CRISPR/dCas9)-based strategy for HIV-1 reservoir purging.
| Main Authors: | , , |
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| Format: | info:ar-repo/semantics/artículo biblioteca |
| Language: | eng |
| Published: |
MDPI
2021-01
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| Subjects: | Retroviridae, Virus de la Inmunodeficiencia Humana, Infección por VIH, Infecciones Latentes, Repeticiones Palindrómicas Cortas Agrupadas y Regularmente Interespaciadas, Transcripción, Lentivirus, Human Immunodeficiency Virus, HIV Infections, Latent Infections, CRISPR, Transcription, |
| Online Access: | http://hdl.handle.net/20.500.12123/9143 https://www.mdpi.com/2076-0817/10/1/16 https://doi.org/10.3390/pathogens10010016 |
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