HIV Cure: New Discovery of 'Seams' Could Lead to Breakthrough

Scientists have finally finished mapping the structure of the protein that encases HIV's genetic information, called a capsid, and have revealed potentially penetrable "seams," U.S News reported.

The entire structure of the virus has never been fully described until the University of Pittsburgh study was published in the journal Nature on Wednesday.

A research team from the University of Pittsburgh School of Medicine used a supercomputer from the University of Illinois name "Blue Waters" to look closely at the virus. The capsid must be tough enough to protect the virus' DNA when it is outside of a host cell, but also needs to be able to break open in order to affect the cell once it has been infected.

"HIV's capsid is stable enough to protect the virus' essential components, but it also has to disassociate once it enters the cell," Peijun Zhang, one of the authors of the study stated. "Understanding the interface by which it disassociates is important to developing new therapies."

Researchers have been trying to penetrate the virus' capsid for years, but it is extremely tough. The new findings may show the weakness in a protein that scientists have been looking for.

"When we saw the structure, we found a very critical interface for the capsid's assembly," said Zhang. "A single amino acid change will lead to the breakdown of it."

According to Zhang the next steps will be to look at two different types of HIV treatment. Researchers can attempt to make the capsid "hyperstable" which would keep the capsid from breaking apart when it tries to infect a cell, most likely rendering the virus harmless to humans.

A second approach could be to make the capsid weaker so that it would not be able to effectively protect the virus' DNA before it would be able to infect a cell. The team discovered a "three-helix bundle" in the capsid that could be targeted by the theoretical drug.

One of the reasons that finding a solid treatment for HIV has been so hard is that the virus mutates very quickly. The team believes that this new approach would target an area that is not as likely to form a resistance.

"Most therapies target the virus' reverse transcriptase," the process that allows the virus to reproduce," Zhang said. "This is another strategy - we can develop drugs against the parts of it that don't mutate as much."