Antibodies show promise fighting strains of HIV
Discovery could be integral in vaccine
LOS ANGELES – An effective vaccine against the AIDS virus may have moved one step closer to reality, researchers said Thursday.
Federal researchers have identified a pair of naturally occurring antibodies that are able to kill more than 90 percent of all strains of the AIDS virus, a finding they say could lead to the development of new treatments for HIV infections and to the production of the first successful vaccine against the virus.
HIV, the virus that causes AIDS, is notoriously mutable, changing the composition of proteins on its surface with ease to escape pressure from the immune system. This enables it to continue infecting cells even after the appearance of antibodies targeting it – and to avoid the relatively ineffective vaccines developed so far.
Hundreds of variants of the virus are now in circulation around the world and the identification of so-called broadly neutralizing antibodies that can block the bulk of them has been the holy grail of HIV researchers.
To date, however, the best antibodies – immune system proteins that fight infections – that researchers have found block only 30 percent to 40 percent of all HIV strains. The identification of antibodies that can block more than 90 percent of strains could lead to what some researchers are dubbing a renaissance in AIDS prevention and treatment.
The key to the new antibodies is that they bind to a site on the virus surface that rarely undergoes mutations.
“I am more optimistic about an AIDS vaccine at this point in time than I have been probably in the last 10 years,” Dr. Gary Nabel of the National Institute of Allergy and Infectious Diseases told Reuters. He led the research reported Thursday in the online edition of the journal Science.
Nabel and his colleagues isolated the antibodies from the blood of a 60-year-old African-American gay man known as Donor 45. Using newly developed imaging and analytical techniques, they found that the two antibodies, called VRC01 and VRC02, bind to a spike on the surface of the virus. This spike interacts with a receptor called the CD4 binding site on the surface of human cells, and when an antibody binds to it, the virus cannot enter a cell.
Because the virus must use CD4 to enter cells, it cannot tolerate mutations in the spike. The composition of the spike is thus pretty much constant in all variants of HIV in circulation.