Scientists crack protein that builds immunity against HIV
Small changes in the protein structure could help patients infected with HIV build the immune system to ensure that the virus does not go on to develop into AIDS, a study has revealed.
Nearly one out of every 300 HIV infected people develop the immune system that recognize and destroy infected cells. In most patients, HIV develops into full-blow AIDS damaging their immune systems.
"I realized that we could create a cohort by going directly to physicians around the world, and I thought we should figure out what is genetically unique about people who do well compared with people who do badly,"
Bruce Walker, an immunologist and director of the Ragon Institute of Massachusetts General Hospital, the Massachusetts Institute of Technology and Harvard University in Charlestown, who led the study.
Walker used a technique called a genome-wide association study to compare the genetic code of 2,600 people with normal HIV infections and the DNA of more than 900 HIV controllers. They found variations in one letter of DNA - at a million points in the genomics of these people. They found more than 300 sites in a region of the genome that codes for proteins involved in immune response, that were associated with control of HIV. Through regression analyses, they narrowed the search to four sites strongly linked to HIV immunity.“This will help us induce better responses to HIV, because we now know what it is that we're trying to induce” said Walker.
The researchers found specific amino acids in the protein HLA-B, earlier linked to diabetes, that differed between controllers and people with normal infections. HLA-B helps in creating immunity in a body against viral attack. "Out of the three billion nucleotides [that make up the human genome], we narrowed it down to a handful of amino acids that define the difference, each coded for by just three nucleotides"
"This confirms that HLA-B is the most important protein", says Rodney Phillips, an immunologist and co-director of the Institute of Emerging Infections at the University of Oxford, UK.
The scientists are bit cautious of how soon a treatment could be devised. "We're a long way from translating this, but the exciting part is that this GWAS led us to an immune response. That has to be good news for vaccines, because they manipulate the immune response," says Walker. "We're cautiously optimistic that this will help us develop ways of inducing better results”.