Tel Aviv, December 18 (ANI/TPS): A tiny viral switch discovered by Israeli and American scientists could open a new front in the fight against antibiotic-resistant infections, a global health threat projected to kill up to 10 million people annually by 2050.
Scientists at the Hebrew University of Jerusalem have revealed that bacteriophages—viruses that infect bacteria—use a small RNA molecule to hijack bacterial cells, a mechanism never described before. The finding offers fresh insights for future phage-based therapies.
The study, led by Sahar Melamed and her team, including PhD student Aviezer Silverman, MSc student Raneem Nashef, and computational biologist Reut Wasserman, was conducted in collaboration with Prof. Ido Golding of the University of Illinois Urbana-Champaign. The research focused on a tiny viral RNA known as PreS.
Unlike most previous research, which concentrated on viral proteins, the study demonstrated that even one of the most extensively studied phages, lambda, uses RNA to directly manipulate bacterial gene expression.
“This small RNA gives the phage another layer of control,” Melamed said. “By regulating essential bacterial genes at exactly the right moment, the virus improves its chances of successful replication. What astonished us most is that phage lambda, studied for more than 75 years, still hides secrets. Discovering an unexpected RNA regulator in such a classic system suggests we have only grasped a single thread of what may be a much richer network of RNA-mediated control in phages.”
The researchers found that PreS acts as a molecular “switch” inside infected bacteria by targeting specific bacterial messenger RNAs. One key target is the message that codes for DnaN, a protein essential for DNA replication. PreS binds to a normally folded region of this mRNA, unfolds it, and makes it easier for the bacterial protein-making machinery to translate it.
The result is increased DnaN production, faster viral DNA replication, and a more efficient infection. When PreS is removed or its binding site is disrupted, the phage weakens, multiplies more slowly, and its destructive phase is delayed.
“This mechanism had never been seen before in phages,” Silverman said. “It shows that even the smallest viral molecules can play a decisive role in infection, giving the virus a subtle but powerful advantage over its host.”
The discovery is particularly striking because small RNAs were not previously considered major players in phage biology. However, PreS is highly conserved across related viruses, suggesting that many phages may share a hidden toolkit of RNA regulators that scientists are only beginning to explore.
Understanding how phages control bacterial cells is critical for both fundamental biology and potential medical applications. With antibiotic resistance rising worldwide, phage therapy—using viruses to selectively attack bacteria—is gaining attention as a flexible and targeted alternative to conventional drugs.
Discoveries such as PreS provide a blueprint for designing smarter phages that are safer, more predictable, and more effective in combating drug-resistant infections.
“Even the smallest viral molecules can have a huge impact on whether an infection succeeds,” Melamed said. “By learning how phages manipulate their hosts at this microscopic level, we can begin to engineer viruses that are both powerful and precise in the fight against antibiotic resistance.”
Beyond medicine, the findings may also have applications in synthetic biology, enabling engineered phages or bacteria to be used in industrial processes, microbiome management, or biofilm control, transforming a once-hidden viral strategy into a versatile tool for health and technology.
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