A new vaccine that uses gene therapy to boost the body’s defenses against tuberculosis (search) may help completely eliminate the bacteria from the body and prevent the disease from coming back.
Researchers say current medications cannot completely rid the body of the bacteria that cause tuberculosis. The remaining bacteria can lie dormant and reactivate many years after therapy and again cause disease.
But a new study shows than an experimental DNA vaccine (search) delivered after chemotherapy completely blocked reactivation of the dormant bacteria in animals and helped prevent a second infection.
If further studies show that the vaccine is effective in humans, it may significantly reduce the number of deaths due to tuberculosis, which is the biggest infectious-disease killer in the world.
New Tuberculosis Vaccine Uses Gene Therapy
In the study, which appears in the current issue of Gene Therapy, researchers studied the effects of the DNA vaccine in mice infected with low doses of the bacteria that cause tuberculosis.
Four weeks after infection, some of the mice were treated with medication, and the rest received the DNA vaccine in addition to medication.
Researchers say the vaccine should induce an immune response from the body to boost its defenses and, therefore, suppress the growth of the tuberculosis bacteria during both the initial infection and later reactivation of dormant bacteria.
The study showed that the vaccine in combination with medication improved the likelihood of completely eliminating the bacteria from the body. In addition, this effect appeared to reduce the risk of repeat infection.
Researchers say this is the first experimental vaccine to demonstrate a protective effect against a secondary tuberculosis infection in animals.
Based on these results, researchers say using the DNA vaccine in combination with medication may be an efficient way to limit further use of medications for tuberculosis and reduce the cost as well as side effects associated with these drugs.
SOURCE: Ha, S. Gene Therapy, Feb. 3, 2005, advance online publication.