Researchers from Cardiff University and University of California (UCLA) conducted a research on HIV-related dementia. Their findings provided clues to the mechanism of the condition. HIV infection can cause mental decline and worsening motor skills. These symptoms are somewhat common. C-C chemokine receptor type 5 (CCR5) is a protein that is highly expressed by T cells and macrophages. This protein is required for viruses such as some strains of HIV to enter and infect host cells. People with specific variations in CCR5 are protected from these strains of HIV. Through random behavioural screen, UCLA researchers noticed that some mutant mice had better memory than others. Further investigation showed that mice with better memory lacked CCR5 in their neurons. In contrast, mice with increased CCR5 had low ability to learn. These data indicated that CCR5 has an impact on learning and memory. In the central nervous system, the protein CCR5 is expressed in microglia, astrocytes and neurons. The researchers assumed that HIV infection could activate CCR5 in neurons, therefore reducing neuron function. Further experiments revealed that HIV seems to cause AIDS-related dementia by elevating the activity of CCR5 in neurons, which impairs the plasticity function of these cells and memory formation. Furthermore, an experimental drug called PRO 140 blocks the HIV co-receptor CCR5 on T cells, which prevents viral entry. What's more, PRO 140 does not seriously affect the normal immune functions mediated by CCR5. This drug is effective in decreasing viral burden in human clinical trials. Based on these information, scientists may be able to develop drugs that target CCR5 on neurons to prevent HIV-related dementia. CusAb offers Recombinant CDHR4.
