phage therapy – BioQuakes

Researchers in Lund have recently discovered an antitoxin mechanism that may be able to protect bacteria against virus attacks by neutralizing hundreds of toxins. Understanding this antitoxin mechanism, named the Panacea, could be the next step to the future success of phage therapy, a treatment for antibiotic resistant infections.

These toxin-antitoxin mechanisms are a kind of on-off switch in bacterial DNA genomes. They are found to attack bacteriophages to defend bacteria.This activation of toxins allows bacteria to “lockdown” and limit growth and spreading of a virus. In order for Phage therapy to be successful in the future, it is important to understand these mechanisms in great depth. The goal of Phage therapy is to use viruses to treat bacterial infections. A toxin dramatically inhibits bacterial growth and an adjacent gene encoding an antitoxin counteracts the toxic effect. Although toxin-antitoxin pairs have been associated with new toxins or antitoxins before, the ability of the Panacea is unprecedented.

As research continues on toxin-antitoxin systems and phage therapy it is clear that what we know is just the tip of the iceberg. As bacteria increasingly become resistant to antibiotics, other approaches are needed to help eliminate infections. The next steps of this research is to continue deepening the understanding of the Panacea and finding toxin-antitoxin systems on a universal scale.

In AP biology class we learned about inhibitors. An inhibitor is something that slows down or prevents a particular reaction or process. A toxin inhibits bacteria from growing and reproducing so the antitoxin can act against the virus that has already spread.

Tevenphage – Photo credit to Wikimedia Commons

While experimenting, a group of scientists noticed that a A virus, VP882, was able to intercept and read the chemical messages between the bacteria to determine when was the best time to strike. Cholera bacteria communicate through molecular signals, a phenomenon known as quorum sensing, to check their population number. The signal in question is called DPO. VP 882, a subcategory of bacteria’s natural predator, the bacteriophage, waits for the bacteria to multiply and is able to check for the DPO. Once there is enough bacteria, in the experiment’s case they observed cholera, the virus multiples and consumes the bacteria like an all-you-can-eat buffet. The scientists tested this by introducing DPO to a mixture of the virus and bacteria not producing DPO and found that that the bacteria was in fact being killed.

The great part about VP 882 is it’s shared characteristic with a plasmid, a ring of DNA that floats around the cell. This makes it easier to possibly genetically engineer the virus so that it will consume other types of bacteria. This entails it can be genetically altered to defeat other harmful bacterial infections, such as salmonella.

Ti plasmid – Photo credit to Wikimedia Commons

Current phage therapy is flawed because phages can only target a single type of bacteria, but infections can contain several types of different bacteria. Patients then need a “cocktail” with a variety of phages, which is a difficult due to the amount of needed testing in order to get approved for usage. With the engineering capability of using a single type of bacteria killer and the ability to turn it to kill bacteria, phage therapy might be able to advance leaps and bounds.

As humans’ storage of effective antibiotics depletes, time is ticking to find new ways to fight bacterial infections. Are bacteriophages and bacteria-killing viruses like VP 882, the answers?

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: phage therapy

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