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Retrovirology. 2014 Dec 11;11:120. doi: 10.1186/s12977-014-0120-x.

BI-2 destabilizes HIV-1 cores during infection and Prevents Binding of CPSF6 to the HIV-1 Capsid.

Author information

1
Department of Microbiology and Immunology, Albert Einstein College of Medicine Bronx, Bronx, NY, 10461, USA. thomas.fricke@einstein.yu.edu.
2
Department of Microbiology and Immunology, Albert Einstein College of Medicine Bronx, Bronx, NY, 10461, USA. cindy.buffone@phd.einstein.yu.edu.
3
Department of Microbiology and Immunology, Albert Einstein College of Medicine Bronx, Bronx, NY, 10461, USA. oppsil82@gmx.de.
4
Department of Microbiology and Immunology, Albert Einstein College of Medicine Bronx, Bronx, NY, 10461, USA. oVaCas@me.com.
5
Department of Microbiology and Immunology, Albert Einstein College of Medicine Bronx, Bronx, NY, 10461, USA. felipe.diaz-griffero@einstein.yu.edu.
6
Albert Einstein College of Medicine, 1301 Morris Park - Price Center 501, New York, NY, 10461, USA. felipe.diaz-griffero@einstein.yu.edu.

Abstract

BACKGROUND:

The recently discovered small-molecule BI-2 potently blocks HIV-1 infection. BI-2 binds to the N-terminal domain of HIV-1 capsid. BI-2 utilizes the same capsid pocket used by the small molecule PF74. Although both drugs bind to the same pocket, it has been proposed that BI-2 uses a different mechanism to block HIV-1 infection when compared to PF74.

FINDINGS:

This work demonstrates that BI-2 destabilizes the HIV-1 core during infection, and prevents the binding of the cellular factor CPSF6 to the HIV-1 core.

CONCLUSIONS:

Overall this short-form paper suggests that BI-2 is using a similar mechanism to the one used by PF74 to block HIV-1 infection.

PMID:
25496772
PMCID:
PMC4271331
DOI:
10.1186/s12977-014-0120-x
[Indexed for MEDLINE]
Free PMC Article

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