A New Antiviral Drug Strategy?
According to wikipedia, there have been drugs targeting CCR5 coreceptor approved for treating HIV. These drugs work by binding to CCR5, thereby prevent binding of HIV and CCR5.

However, drug resistance can still develop. Some HIV can bypass it by shifting tropism to CXCR4. While others can increase its affinity to CCR5.

And some receptors are vital for the functions of cells. If we design drugs to these targets, we should make sure that the drugs only prevent binding of viruses specifically without disrupting their normal functions.


  Maraviroc was approved for use by the FDA in August 2007.It is the
  only one thus far approved by the FDA for clinical use, thus becoming
  the first CCR5 inhibitor. A 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.
  https://en.m.wikipedia.org/wiki/CCR5


http://www.ncbi.nlm.nih.gov/pubmed/11782552
http://www.sciencedirect.com/science/article/pii/S0042682206008245