- Top of page
- Chemokine receptor use corresponds to HIV-1 biological phenotype
- Chemokine receptor signalling in HIV-1 infection
- Evolution of HIV-1 coreceptor use during pathogenesis
- What determines HIV-1 coreceptor switch?
- Increased emergence of CXCR4 use: sign of an evolving epidemic?
- Intra-patient evolution of the CCR5-restricted HIV-1 phenotype
- Modifications of Env structures as the molecular rationale for in vivo R5 phenotypic evolution
- Chimeric CCR5/CXCR4 receptors as a tool to predict HIV-1 sensitivity to entry inhibitors
- The way to individualized drug choice
- Conflict of interest statement
- Supporting Information
Abstract. Fenyö EM, Esbjörnsson J, Medstrand P, Jansson M (Division of Medical Microbiology, Lund; Lund University, Lund; and Karolinska Institutet, Stockholm, Sweden). Human immunodeficiency virus type 1 biological variation and coreceptor use: from concept to clinical significance (Symposium). J Intern Med 2011; doi: 10.1111/j.1365-2796.2011.02455.x
There is ample evidence for intra-patient evolution of the human immunodeficiency virus type 1 (HIV-1) biological phenotype during the pathogenic process. Evolution often involves switch of coreceptor use from CCR5 to CXCR4, but change to more flexible use of CCR5 occurs over time even in patients with maintained CCR5 use. The increasing use of entry inhibitors in the clinic, often specific for one or the other HIV-1 coreceptor or with different binding properties to CCR5, calls for virus testing in patients prior to treatment initiation. Cell lines expressing CCR5/CXCR4 chimeric receptors are tools for testing viruses for mode of CCR5 use. It is conceivable that small-molecule entry inhibitors that differentially bind to CCR5 can be matched for best effect against HIV-1 with different modes of CCR5 use, thereby allowing an individualized drug choice specifically tailored for each patient.