Balance between Retroviral Latency and Transcription: Based on HIV Model

Pathogens

卷:10

CésarN. Cortés-Rubio¹  JuanP. Jaworski²  Aneta Pluta³ 

[1] Centre for Research in Infectious Diseases, National Institute of Respiratory Diseases, Tlalpan 4502, 14080 Mexico City, Mexico;

[2] Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET), Instituto Nacional de Tecnología Agropecuaria (INTA), Instituto de Virología, Nicolás Repetto y De los Reseros (s/n), CP1686 Hurlingham, Buenos Aires, Argentina;

[3] Department of Biochemistry, National Veterinary Research Institute, 24-100 Puławy, Poland;

关键词: retroviruses;    human immunodeficiency virus type 1;    HIV-1;    terminal repeat region;    LTR;    regulation transcription;   

DOI  :  10.3390/pathogens10010016

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown