Passive Repression of HIV-1 Long Terminal Repeat Enhancer Controlled Viral Transcription in HIV-1 Infected Cells by Cationic DNA-Binding Fusion Proteins

2001 ◽  
pp. 988-989
Author(s):  
S. R. K. Hoffmann ◽  
L. Bisset ◽  
J. Schüpbach ◽  
B. Gutte
2019 ◽  
Vol 116 (6) ◽  
pp. 2282-2289 ◽  
Author(s):  
Manabu Taura ◽  
Eric Song ◽  
Ya-Chi Ho ◽  
Akiko Iwasaki

HIV-1 integrates into the genome of target cells and establishes latency indefinitely. Understanding the molecular mechanism of HIV-1 latency maintenance is needed for therapeutic strategies to combat existing infection. In this study, we found an unexpected role for Apobec3A (apolipoprotein B MRNA editing enzyme catalytic subunit 3A, abbreviated “A3A”) in maintaining the latency state within HIV-1–infected cells. Overexpression of A3A in latently infected cell lines led to lower reactivation, while knockdown or knockout of A3A led to increased spontaneous and inducible HIV-1 reactivation. A3A maintains HIV-1 latency by associating with proviral DNA at the 5′ long terminal repeat region, recruiting KAP1 and HP1, and imposing repressive histone marks. We show that knockdown of A3A in latently infected human primary CD4 T cells enhanced HIV-1 reactivation. Collectively, we provide evidence and a mechanism by which A3A reinforces HIV-1 latency in infected CD4 T cells.


2010 ◽  
Vol 65 (3) ◽  
pp. 434-437 ◽  
Author(s):  
Sandrine Reigadas ◽  
Marie-Line Andréola ◽  
Linda Wittkop ◽  
Ophélie Cosnefroy ◽  
Guerric Anies ◽  
...  

2004 ◽  
Vol 1030 (1) ◽  
pp. 636-643 ◽  
Author(s):  
GIULIA MARSILI ◽  
ANNA LISA REMOLI ◽  
MARCO SGARBANTI ◽  
ANGELA BATTISTINI

AIDS ◽  
1995 ◽  
Vol 9 (7) ◽  
pp. 675-684 ◽  
Author(s):  
Mounir Ait-Khaled ◽  
James E. McLaughlin ◽  
Margaret A. Johnson ◽  
Vincent C. Emery

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