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Trends Mol Med. 2018 May;24(5):507-520. doi: 10.1016/j.molmed.2018.03.004. Epub 2018 Mar 30.

A New Class of Antiretroviral Enabling Innate Immunity by Protecting APOBEC3 from HIV Vif-Dependent Degradation.

Author information

1
OyaGen, Inc., 77 Ridgeland Road, Rochester, NY 14623, USA. Electronic address: rbennett@oyageninc.com.
2
OyaGen, Inc., 77 Ridgeland Road, Rochester, NY 14623, USA.
3
OyaGen, Inc., 77 Ridgeland Road, Rochester, NY 14623, USA; University of Rochester, School of Medicine and Dentistry, Department of Biochemistry and Biophysics, 601 Elmwood Avenue, Rochester, NY 14642, USA. Electronic address: harold.smith@rochester.edu.

Abstract

The infectivity of HIV depends on overcoming APOBEC3 (A3) innate immunity, predominantly through the expression of the viral protein Vif, which induces A3 degradation in the proteasome. Disruption of the functional interactions of Vif enables A3 mutagenesis of the HIV genome during viral replication, which can result in a broadly neutralizing antiviral effect. Vif function requires self-association along with interactions with A3 proteins, protein chaperones, and factors of the ubiquitination machinery and these are described here as a potential platform for novel antiviral drug discovery. This Review will examine the current state of development of Vif inhibitors that we believe to have therapeutic and functional cure potential.

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