Abstract
CCR5 and its interaction with chemokine ligands have been crucial for understanding and tackling HIV-1 entry into target cells. However, over time, CCR5 has witnessed an impressive transition from being considered rather unimportant in physiology and pathology to becoming central in a growing number of pathophysiological conditions. It now turns out that the massive efforts devoted to combat HIV-1 entry by interfering with CCR5, and the subsequent production of chemokine ligand variants, small chemical compounds, and other molecular entities and strategies, may set the therapeutic standards for a wealth of different pathologies. Expressed on various cell types, CCR5 plays a vital role in the inflammatory response by directing cells to sites of inflammation. Aside HIV-1, CCR5 has been implicated in other infectious diseases and non-infectious diseases such as cancer, atherosclerosis, and inflammatory bowel disease. Individuals carrying the CCR5Δ32 mutation live a normal life and are warranted a natural barrier to HIV-1 infection. Therefore, CCR5 antagonism and gene-edited knockout of the receptor gained growing interest for the therapeutic role that CCR5 blockade may play in the attenuation of the severity or progression of numerous diseases.
Highlights
From its discovery, CCR5 has been a key player in HIV-1 entry into target cells and, together with its chemokine ligands, helped in understanding and tackling HIV-1 infection [1, 2]
CCR5 predominates among the chemokine co-receptors used by HIV-1 for cell entry, and R5-tropic HIV-1 strains are those most commonly transmitted in the early stages of infection
In this mini-review, we describe several aspects related to the pathophysiology of CCR5, discuss its possible dispensability, and analyze its blockade as a comprehensive therapeutic perspective
Summary
CCR5 has been a key player in HIV-1 entry into target cells and, together with its chemokine ligands, helped in understanding and tackling HIV-1 infection [1, 2]. CCR5 predominates among the chemokine co-receptors used by HIV-1 for cell entry, and R5-tropic HIV-1 strains are those most commonly transmitted in the early stages of infection. A 32 base pair deletion within the CCR5 gene leads to a non-functional gene product that does not reach the cell surface, and subjects with a homozygous CCR5Δ32 deletion are protected from HIV-1 infection [3].
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