What might explain why jill but not jack shows efficacy

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Reference no: EM133670171

Question: The CCR5 receptor is a GPCR that acts as a "co-receptor" for HIV entry, which means the virus binds to receptor and uses it to gain entry into the cell. Humans that carry a mutation in the CCR5 receptor that prevent the proper folding and secretion of the CCR5 receptor to the plasma membrane are resistant to HIV infection. Based on this finding, you do a screen for new ANTAGONIST ligands at the CCR5 receptor in hopes that they will function as novel anti-HIV drugs that block HIV entry into cells. You identify two new ligands Jack and Jill. Neither Jack nor Jill have any effect on basal receptor activity. Both Jack and Jill have the same affinity at the CCR5 receptor. Both have equivalent potency at blocking G protein activation by all the endogenous ligands of the CCR5 receptor, CCL3, 4, and 5. However, only Jill effectively blocks HIV entry in your cell-based model for cell entry and infection. What might explain why Jill but not Jack shows efficacy for blocking HIV entry?

Reference no: EM133670171

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