09-25-2009, 05:22 AM
"A number of new experimental HIV drugs, called entry inhibitors, have been designed to interfere with the interaction between CCR5 and HIV, including PRO140 (Progenics), Vicriviroc (Schering Plough), Aplaviroc (GW-873140) (GlaxoSmithKline) and Maraviroc (UK-427857) (Pfizer). A potential problem of this approach is that, while CCR5 is the major co-receptor by which HIV infects cells, it is not the only such co-receptor. It is possible that under selective pressure HIV will evolve to use another co-receptor. However, examination of viral resistance to AD101, molecular antagonist of CCR5, indicated that resistant viruses did not switch to another coreceptor (CXCR4) but persisted in using CCR5, either through binding to alternative domains of CCR5, or by binding to the receptor at a higher affinity. Development of Aplaviroc has been terminated due to safety concerns (potential liver toxicity)"
http://en.wikipedia.org/wiki/CCR5
Most important is that we have discovered a key mechanism for many infectious diseases. So, theoretically, if we can understand the role of CCR5, then we can provide resistance and cures for many other recombinant diseases such as Smallpox, Ebola, Yersinia pestis, Marburg, influenza, or papillomavirus.
http://en.wikipedia.org/wiki/CCR5
Most important is that we have discovered a key mechanism for many infectious diseases. So, theoretically, if we can understand the role of CCR5, then we can provide resistance and cures for many other recombinant diseases such as Smallpox, Ebola, Yersinia pestis, Marburg, influenza, or papillomavirus.