CCR5Δ32 mutation and HIV infection: basis for curative HIV therapy

Kristina Allers; Thomas Schneider

doi:10.1016/j.coviro.2015.06.007

CCR5Δ32 mutation and HIV infection: basis for curative HIV therapy

Curr Opin Virol. 2015 Oct:14:24-9. doi: 10.1016/j.coviro.2015.06.007. Epub 2015 Jul 1.

Authors

Kristina Allers¹, Thomas Schneider²

Affiliations

¹ Department of Gastroenterology, Infectious Diseases, and Rheumatology, Campus Benjamin Franklin, Charité-Universitätsmedizin, Berlin, Germany. Electronic address: kristina.allers@charite.de.
² Department of Gastroenterology, Infectious Diseases, and Rheumatology, Campus Benjamin Franklin, Charité-Universitätsmedizin, Berlin, Germany.

PMID: 26143158
DOI: 10.1016/j.coviro.2015.06.007

Abstract

The C-C chemokine receptor 5 (CCR5) is expressed on potential human immunodeficiency virus (HIV) target cells and serves as the predominant co-receptor for viral entry during initial transmission and through the early stages of infection. A homozygous Δ32 mutation in the CCR5 gene prevents CCR5 cell surface expression and thus confers resistance to infection with CCR5-tropic HIV strains. Transplantation of hematopoietic stem cells from a CCR5Δ32/Δ32 donor was previously successful in eliminating HIV from the recipient's immune system, suggesting that targeted CCR5 disruption can lead to an HIV cure. Therefore, intense work is currently being carried out on CCR5 gene-editing tools to develop curative HIV therapy. Here, we review the natural function of CCR5, the progress made on CCR5 gene editing to date and discuss the current limitations.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Genetic Therapy / methods*
HIV / physiology
HIV Infections / therapy*
Humans
Receptors, CCR5 / genetics*
Receptors, HIV / genetics*
Sequence Deletion*
Stem Cell Transplantation / methods*
Virus Internalization

Substances

CCR5 protein, human
Receptors, CCR5
Receptors, HIV