Journal
VIRUSES-BASEL
Volume 2, Issue 5, Pages 1069-1105Publisher
MDPI
DOI: 10.3390/v2051069
Keywords
HIV-1; envelope; gp120; V3 loop; gp41; CCR5; maraviroc; vicriviroc
Categories
Funding
- NIH [AI49170]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI049170, R56AI049170, R21AI049170] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007250] Funding Source: NIH RePORTER
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Entry inhibitors represent a new class of antiretroviral agents for the treatment of infection with HIV-1. While resistance to other HIV drug classes has been well described, resistance to this new class is still ill defined despite considerable clinical use. Several potential mechanisms have been proposed: tropism switching ( utilization of CXCR4 instead of CCR5 for entry), increased affinity for the coreceptor, increased rate of virus entry into host cells, and utilization of inhibitor-bound receptor for entry. In this review we will address the development of attachment, fusion, and coreceptor entry inhibitors and explore recent studies describing potential mechanisms of resistance.
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