Study On The Trafficking Mechanism Of HIV-1 Coreceptor CCR5

In this study, a truncated allele of CCR5 was cloned from Han nationalityChinese, which showed a deletion in the C-terminal region from the 309thresidue andchanged at the 299th residue. But further investigation showed that people ofheterozygotes carrying this truncated allele had no obvious health problems. Wethereafter constructed two sets of expressional constructs for CCR5/CCR5-893(-)using pcDNA3 and pIND plamids, which were then treated with PHA. The membraneand cytoplasm expression were detected by flow cytometry. The rescue of membranepresentation of CCR5-893(-) was observed when under inducement of PHA. Itsuggested a factor(s) induced by PHA could help the trafficking of CCR5-893(-). Thesubcellular staining of the CCR5 or/and CCR5-893(-) detected by confocalmicroscopy confirmed the observation by flow cytometry. We also observedsaturation for the membrane expression of CCR5 and CCR5-893(-) using theinducible expression system of pIND, which indicated there existed a limiting factor(s)for the presentation of CCR5. Suggestion of the mechanism for CCR5 trafficking tocell surface was put forward in this study. The study of the CCR5 trafficking to cellmembrane will provide another selective target for anti-HIV therapy based onintervention of CCR5.