Great question! I looked around and couldn’t find any literature specifically on this topic. I imagine bacteria could definitely adapt and inhibit the portal protein. It could potentially be bound in the pore, to stop the flow of DNA.
A major advantage of phage therapy is its specificity to treat resistant infections. Often bacteria can become resistant to a wide range of antibiotics. Hence, phage therapy can be engineered to specifically attack a certain strain. It also has minimal impact on human cells or healthy bacteria.
In most of the papers that I read, all bacteriophages should have portal proteins (to my knowledge). There may be some strange bacteriophage without it, but I’m not really sure how that phage could function.
Good question. You would “target” it by making a small change to the phage genome sequence and changing one or multiple residues in the portal protein to make it more effective.
Are there any bacterial adaptations or evolutions that combat this phage entry via these portal proteins?
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Great question! I looked around and couldn’t find any literature specifically on this topic. I imagine bacteria could definitely adapt and inhibit the portal protein. It could potentially be bound in the pore, to stop the flow of DNA.
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What is the advantage of using this phage over traditional antibiotics?
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A major advantage of phage therapy is its specificity to treat resistant infections. Often bacteria can become resistant to a wide range of antibiotics. Hence, phage therapy can be engineered to specifically attack a certain strain. It also has minimal impact on human cells or healthy bacteria.
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Are there any phages that you know of that don’t have this portal protein?
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In most of the papers that I read, all bacteriophages should have portal proteins (to my knowledge). There may be some strange bacteriophage without it, but I’m not really sure how that phage could function.
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I liked your poster a lot, it looks super nice. How would you target the portal protein?
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Good question. You would “target” it by making a small change to the phage genome sequence and changing one or multiple residues in the portal protein to make it more effective.
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