HIV-1 replication in human immune cells is independent of TAR DNA binding Protein 43 (TDP-43) expression.
    
    
        
    
    
        
        PLoS ONE 9:e105478 (2014)
    
    
    
      
      
	
	    The TAR DNA binding protein (TDP-43) was originally identified as a host cell factor binding to the HIV-1 LTR and thereby suppressing HIV-1 transcription and gene expression (Ou et al., J.Virol. 1995, 69(6):3584). TDP-43 is a global regulator of transcription, can influence RNA metabolism in many different ways and is ubiquitously expressed. Thus, TDP-43 could be a major factor restricting HIV-1 replication at the level of LTR transcription and gene expression. These facts prompted us to revisit the role of TDP-43 for HIV-1 replication. We utilized established HIV-1 cell culture systems as well as primary cell models and performed a comprehensive analysis of TDP-43 function and investigated its putative impact on HIV-1 gene expression. In HIV-1 infected cells TDP-43 was neither degraded nor sequestered from the nucleus. Furthermore, TDP-43 overexpression as well as siRNA mediated knockdown did not affect HIV-1 gene expression and virus production in T cells and macrophages. In summary, our experiments argue against a restricting role of TDP-43 during HIV-1 replication in immune cells.
	
	
	    
	
       
      
	
	    
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        Publication type
        Article: Journal article
    
 
    
        Document type
        Scientific Article
    
 
    
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        Keywords
        Human-immunodeficiency-virus; T-cells; Restriction Factors; Nuclear Factor; Nef; Release; Rna; Vpu; Transcription; Macrophages
    
 
    
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        Language
        english
    
 
    
        Publication Year
        2014
    
 
    
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        HGF-reported in Year
        2014
    
 
    
    
        ISSN (print) / ISBN
        1932-6203
    
 
    
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	    Volume: 9,  
	    Issue: 8,  
	    Pages: ,  
	    Article Number: e105478 
	    Supplement: ,  
	
    
 
    
        
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            Publisher
            Public Library of Science (PLoS)
        
 
        
            Publishing Place
            Lawrence, Kan.
        
 
	
        
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        Reviewing status
        Peer reviewed
    
 
     
    
        POF-Topic(s)
        30203 - Molecular Targets and Therapies
30204 - Cell Programming and Repair
    
 
    
        Research field(s)
        Immune Response and Infection
Genetics and Epidemiology
    
 
    
        PSP Element(s)
        G-502700-006
G-502700-001
G-500500-001
    
 
    
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        Erfassungsdatum
        2014-08-17