Abstract

CCR5 and CXCR4 are chemokine receptors recognize by HIV to enter into the host cell. In this review, we focus on their biology, function and pivotal role in HIV-1 infection, and also, how HIV quasi-species change tropism depending on their expression on the cell surface. We also discuss about the state-of-the-art strategies for targeting CCR5 and CXCR4, with emphasis on novel gene therapies that mimic a natural mutation called CCR5-delta32, enabling innate protection against HIV R5 strains. Trials with gene therapies can knockout both co-receptors and confer protection in vitro without mutants. These techniques include zinc finger nucleases (ZFN), clustered regularly interspaced palindromic repeats/CRISPR-associated protein 9 nuclease (CRSIRP/Cas9), transcription activator-like effectors nuclease (TALEN), short hairpin RNA (shRNA), and ribozymes.

Authors and Affiliations