A New Class of Antiretroviral Enabling Innate Immunity by Protecting APOBEC3 from HIV Vif-Dependent Degradation
| Autor: | Harold C. Smith, Ryan P. Bennett, Jason D. Salter |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Viral protein medicine.drug_class viruses HIV Infections Biology medicine.disease_cause Article Cytosine Deaminase 03 medical and health sciences Ubiquitin Immunity Cytidine Deaminase vif Gene Products Human Immunodeficiency Virus medicine Humans APOBEC Deaminases Molecular Biology Innate immune system 030102 biochemistry & molecular biology virus diseases Cytidine deaminase biochemical phenomena metabolism and nutrition Virology Immunity Innate 030104 developmental biology Anti-Retroviral Agents Proteasome Viral replication Host-Pathogen Interactions Proteolysis HIV-1 biology.protein Molecular Medicine Antiviral drug Protein Binding |
| Zdroj: | Trends Mol Med |
| ISSN: | 1471-4914 |
| Popis: | The infectivity of the human immunodeficiency virus (HIV) depends on overcoming APOBEC3 (A3) innate immunity and does so 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 article will examine the current state of development of Vif inhibitors that we believe to have therapeutic and functional cure potential. |
| Databáze: | OpenAIRE |
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