by Alicia M Prater PhD

Created on: October 03, 2007   Last Updated: August 16, 2010

The quest for an HIV vaccine is a road paved with failure. However, recent research has found that pessimism about the possibility of a vaccine may need to be re-thought.

Vaccines work by exposing the body's immune system to specific pieces of an infectious agent, such as a virus. This exposure primes the immune response - when an individual is exposed to the real virus the body already has an immune response in the form of antibodies against it and it is killed before it can infect the host cells. The problem with HIV, the human immunodeficiency virus, in this context is that the proteins on its surface, the most useful and common targets of antibodies, undergo constant mutation. Even in the same individual the virus is different when comparing the strain that initially infected them and the strain present when they develop AIDS, a syndrome of opportunistic infections that take advantage of the immune deficiency caused by HIV infection. This high mutation rate is one way HIV overcomes our immune system. This high mutation rate has also made the quest for an HIV vaccine very difficult, leaving a number of stalled clinical trials in its wake.

Early in HIV research, some researchers focused on defects in particular co-receptors that protect some populations, particularly in Scandinavia, from HIV infection. Targeting this weakness in the virus was though to be key to new prevention methods, and possibly a key to a vaccine. However, different strains of HIV are capable of infecting different immune cells more efficiently than others. Targeting the appropriate people who will come into contact with a particular strain would be difficult. Also, there are now individuals exhibiting the cumulative effects of being infected with multiple strains of HIV. How would a single vaccine protect against the spread of this pathogen?

Broadly neutralizing antibodies were discovered in the blood of HIV-infected patients a few years ago. These rare, but broadly affective antibodies target proteins on the viral surface that do not vary as much between virus molecules. These are namely the glycoproteins that assist in the binding and internalization of the virus to the host cell (gp120 in the CD4 binding site and gp41 in cell fusion and entry; Sun et al. NIH) found that broadly neutralizing antibodies VRC01 and VRC02 are effective against 90 percent of known circulating HIV strains.

These findings are the most promising to date for a vaccine against HIV, but still not good enough. There is still much work to be done to take the knowledge gained in researching these antibodies and create a composite, synthetic vaccine that can protect almost all of the people who receive it. Saying that the vaccine is on the horizon is a bit of a stretch, but the light is definitely shining - researchers are no longer stumbling in the dark.

However, the key to ridding the world of HIV infection is still prevention. Since 1981 the virus has been attributed to the deaths of more than 25 million people, and another 30 million are currently infected (AVERT).

Learn more about this author, Alicia M Prater PhD.
Click here to send this author comments or questions.