Researchers at the Weizmann Institute of Science in Rehovot have made a significant discovery regarding a novel immune mechanism that uses a family of proteins to deplete cells of their energy, thus protecting them from invasive pathogens. This mechanism is found across a wide range of living creatures, from single-celled organisms to more complex beings like bees and corals. This energy-depleting strategy prevents pathogens from replicating by cutting off their access to the main energy “currency” of cells, adenosine triphosphate (ATP).
The scientists primarily focused on studying how bacteria defend themselves against bacteriophages, which are viruses that attack bacteria. They discovered a gene that encodes a protein capable of breaking down ATP molecules. By doing so, the immune system effectively starves the invading bacteriophage of the energy it needs to reproduce. In the absence of this gene, the viruses replicated at an accelerated rate.
Dr. François Rousset, who led the research team, noted the brilliance of the strategy, explaining that when a bacterium is already infected and close to dying, it’s advantageous to deplete its own energy reserves, preventing the virus from spreading further.
Interestingly, the researchers found that this immune strategy is more widespread than initially thought. They identified over 1,000 immune genes across various bacteria that work similarly by depleting ATP. This mechanism was even present in organisms like fungi, insects (such as bees), corals, and sponges. Although humans lack this specific immune protein, the researchers believe it could be an ancient precursor to the proteins involved in our innate immune system.
This study not only sheds light on the immune strategies of diverse organisms but also highlights the interconnectedness of immune mechanisms across different levels of complexity in the living world. By understanding how ATP molecules play a role in immunity, researchers gain insights into the defense strategies that countless organisms employ when combating viral attacks.
