In vitro and In vivo Resistance to Human Immuno Deficiency Virus Type 1 Entry Inhibitors
4Transfusion transmitted Diseases Center, Institute of Blood Transfusion, Chinese Academy of Medical Science, #26 Hua-Cai Road, Long-Tan-Si Industrial Park, Chenghua District, Chengdu, 610052 Sichuan Province, P. R. China
- *Corresponding Author:
- Keisuke Yusa
Division of Biological Chemistry and Biologicals
National Institute of Health Sciences, Kami-youga 1-18-1
Setagaya, Tokyo 158-8501, Japan
Tel: +81-3-3700-1141 ext. 335
E-mail: [email protected]
Received Date: October 18, 2011; Accepted Date: December 02, 2011; Published Date: December 05, 2011
Citation: Maeda R, Yoshimura K, Miyamoto F, Kodama E, Harada S, et al. (2011) In vitro and In vivo Resistance to Human Immunodeficiency Virus Type 1 Entry Inhibitors. J AIDS Clinic Res S2:004. doi:10.4172/2155-6113.S2-004
Copyright: © 2011 Maeda R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Viral entry is one of the most important targets for the efficient treatment of Human immunodeficiency virus type 1 (HIV-1)-infected patients. The entry process consists of multiple molecular steps: attachment of viral gp120 to CD4, interaction of gp120 with CCR5 or CXCR4 co-receptors, and gp41-mediated fusion of the viral and cellular membranes. Understanding the sequential steps of the entry process has enabled the production of various antiviral drugs to block each of these steps. Currently, the CCR5 inhibitor, maraviroc, and the fusion inhibitor, enfuvirtide, are clinically available. However, the emergence of HIV-1 strains resistant to entry inhibitors, as commonly observed for other classes of antiviral agents, is a serious problem. In this review, we describe a variety of entry inhibitors targeting different steps of viral entry and escape variants that are generated in vitro and in vivo.