A virus kills a bacterium, and in the wreckage, other microbes may find one of life’s most essential nutrients: vitamin B12.
New research from Virginia Tech suggests that bacteriophages, viruses that infect bacteria, can release vitamin B12 trapped inside bacterial cells. That sudden nutrient windfall can then fuel neighboring microbes that cannot make B12 themselves, reshaping the wider community in the process.
Vitamin B12, also known as cobalamin, is required for critical biological processes, including DNA synthesis, red blood cell formation, and normal nerve function. Yet its origins are unusually exclusive. Humans, animals, and plants cannot manufacture it. Only certain bacteria and archaea have the machinery needed to produce it.
How Viruses Unlock Vitamin B12
Making B12 is also metabolically expensive, and only a minority of microorganisms can do it. Many others have evolved to obtain B12 or closely related compounds, called cobamides, from their surroundings instead. This dependence occurs across microbial ecosystems in the oceans, soil, and the mammalian gut.
That creates a biological puzzle. If B12 is costly to make and valuable to the cell producing it, why would enough of the vitamin end up outside those cells to sustain their neighbors?
The study, published in The ISME Journal, points to an unexpectedly violent answer.
Why B12 Stays Trapped in Bacteria
Bacteriophages, usually shortened to phages, infect bacteria. They are widespread wherever bacteria live and can strongly influence microbial communities, including those in the human gut.
During a lytic infection, a phage attaches to a bacterial cell and inserts its genetic material. The virus then hijacks the bacterium’s molecular machinery to manufacture new copies of itself. Eventually, the host cell ruptures.
The newly produced phages escape, but they are not the only things released. DNA, proteins, sugars, and other molecules that had been locked inside the bacterium spill into the surrounding environment.
“It has all the DNA, the protein, sugars, all these things that the bacterial cell normally hoards so that it can continue to grow,” Virginia Tech biologist Bryan Hsu said.
Phages Turn Bacteria Into Nutrient Sources
The researchers found that vitamin B12 can be part of that cellular bounty.
Hsu and his colleagues tested the idea using a controlled system containing a bacterium capable of producing B12 and another bacterium that needed the vitamin but could not make enough for itself.
When the B12 producer remained intact, the dependent bacterium failed to grow. The vitamin existed, but it was effectively locked away.
Once the researchers introduced a phage that destroyed the producer cells, the situation changed. B12 escaped into the environment at concentrations sufficient to support the other bacteria.
“In a genetically well-defined system, we can demonstrate that phage is necessary,” Hsu said. “The B12 doesn’t just leak out.”
Testing Whether B12 Drives Microbial Growth
A ruptured bacterium releases thousands of different cellular components, so the researchers needed to show that B12 itself was responsible for the growth.
David da Silva Barreira, the study’s first author and a former Virginia Tech postdoctoral associate, repeated the experiment using a genetically modified bacterial strain that could not produce B12.
Phages still destroyed those bacteria, releasing their internal contents. But this time the B12-dependent microbes did not grow.
That result showed that simply bursting a bacterial cell was not enough. B12 was the critical resource supporting the neighboring microbes.
B12 Release Reshapes Gut Bacteria
The team then moved beyond the simplified laboratory pairing and tested major groups of bacteria associated with the human digestive tract. Once again, B12-dependent gut bacteria benefited when phages lysed B12-producing cells.
The effects extended beyond individual species. According to the study, phage-released B12 produced significant changes in the composition of bacterial communities and increased their diversity. When researchers simply added B12 directly to the growth medium, that diversity effect was reduced, suggesting that the timing and location of nutrient release may matter alongside the nutrient itself.
Phages are often described mainly in terms of the bacteria they kill. The new findings highlight another side of that relationship.
When a virus destroys one microbe, the contents of that cell do not disappear. They become resources that other organisms can potentially use. In that sense, phages may act as microscopic nutrient recyclers, transferring valuable molecules from organisms that manufacture them to organisms that depend on scavenging.
A Wider Role for Viruses in Microbial Ecosystems
The idea may extend well beyond the gut. Cobamides such as B12 are exchanged among organisms in environments ranging from soil to the ocean, and previous research has also found phage-mediated B12 release in marine microbial systems.
That gives viral infection an ecological role that is easy to overlook. A phage may kill its immediate bacterial host while indirectly helping unrelated microbes nearby.
For the gut microbiome, the findings suggest that viruses could influence the community not only by deciding which bacteria survive but also by changing who gets access to scarce nutrients.
Reference: “Bacteriophage-mediated cell lysis externalizes a metabolically valuable nutrient to broadly modulate bacterial communities” by David da Silva Barreira, Hannah M Poole, Rogério A Bataglioli and Bryan B Hsu, 23 June 2026, The ISME Journal.
DOI: 10.1093/ismejo/wrag160
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