Scientists at NYU Langone Medical Center have found that "immune evasion", which is common to many viruses, bacteria and parasites, is uncommon to M. tuberculosis where the antigens remain strikingly unchanged and homogenous.
The study suggests that M. tuberculosis antigens do not mutate because they hope to be recognized by the body's immune system- perhaps because the host immune mechanism that leads to the typical lung destruction and cough can contribute to the spread of the disease.
The discovery could change the direction of vaccine research and eventually result in a new focus on different targets of immune response to the bacteria.
"The finding that the tuberculosis bacterium acts completely differently from other pathogens is quite surprising and unexpected. If you get infected with the influenza virus, for example, the body's immune system recognizes it and tends to eliminate it. In tuberculosis, our immune response doesn't get rid of it - it tends to hold on to it for a while - keeping the bacteria under partial control," Nature quoted Dr. Joel Ernst, lead author of the study, as saying.
The study found that instead of "suffering" from being recognized, recognition of tuberculosis antigens actually benefit the bacteria - and it is this recognition that helps the bacteria to be transmitted from person to person.
For the study, scientists used a novel high-throughput DNA sequencing method to analyze the whole genomes of 22 clinical strains of M. tuberculosis from different parts of the world.
They then determined that the number of and type of mutations that occurred in antigens is much lower compared to other regions of the M. tuberculosis genome.
The study was published in Nature Genetics.