Abstract

It is now well established that an array of CC and CXC chemokine receptors, in association with the CD4 molecule, can interact with the HIV-1 gp120 protein to facilitate viral fusion. A 32bp deletion in the CC chemokine receptor CCR5, the major M-tropic viral co-receptor, provides considerable protection against HIV-1 transmission and has been associated with a delay in disease progression. The effects of the Δ32 allele appear to be mediated through the phenotype of CCR5 expression as opposed to genotype. Here we discuss the potential effects that the Δ32 allele and other polymorphisms in the chemokine receptor repertoire may have on both HIV-1 transmission and disease progression.

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