scholarly journals Cell-Specific RNA Aptamer against Human CCR5 Specifically Targets HIV-1 Susceptible Cells and Inhibits HIV-1 Infectivity

2015 ◽  
Vol 22 (3) ◽  
pp. 379-390 ◽  
Author(s):  
Jiehua Zhou ◽  
Sangeetha Satheesan ◽  
Haitang Li ◽  
Marc S. Weinberg ◽  
Kevin V. Morris ◽  
...  
Keyword(s):  
2013 ◽  
Vol 32 (8) ◽  
pp. 1202-1210 ◽  
Author(s):  
Nejla Stambouli ◽  
Ning-Ning Wei ◽  
Asma Jlizi ◽  
Samah Aissa ◽  
Rim Abdelmalek ◽  
...  

2001 ◽  
Vol 11 (24) ◽  
pp. 3103-3106 ◽  
Author(s):  
Dooseop Kim ◽  
Liping Wang ◽  
Charles G. Caldwell ◽  
Ping Chen ◽  
Paul E. Finke ◽  
...  

2021 ◽  
Author(s):  
Maria E Cardona ◽  
Jorma Hinkula ◽  
Kristin Gustafsson ◽  
Birger Christensson ◽  
Britta Wahren ◽  
...  

Abstract Treatment with RNAi against HIV-1 transcripts efficiently inhibits viral replication but induces selection of escape mutants; therefore, the CCR5 coreceptor was suggested as an additional target. Blocking viral and host transcripts improved the antiviral effect. We have used short hairpin RNA (shRNA) targeting the human CCR5 (shCCR5) or the HIV-1 rev (shRev) transcripts to demonstrate distinctive properties of anti-CCR5 shRNA: shCCR5 induced more sustained protection than shRev; partial reduction in CCR5 expression substantially decreased HIV-1 infection, and shCCR5 performed better than shRev in the mixed shRNA-treated and untreated cultures. These observations indicate that CCR5 inhibitors should be conveniently included in HIV-1 gene silencing treatment schedules when only a certain cell fraction is protected to further reduce endogenous virus in a properly ART-treated HIV-1 infected individual.


2017 ◽  
Vol 53 (52) ◽  
pp. 7056-7059 ◽  
Author(s):  
Yudai Yamaoki ◽  
Takashi Nagata ◽  
Tsukasa Mashima ◽  
Masato Katahira

The development of the first K+-responsive RNA aptamer demonstrating ON/OFF switching of its target-binding activity by sensing the addition/removal of K+ is reported.


Author(s):  
M. S. Radhi ◽  
A. R. Ruslinda ◽  
M. F. Fatin ◽  
Saeed S. Ba Hashwan ◽  
M. K. Md. Arshad ◽  
...  

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