Tag Archives: bacteriophage

Should I Stay or Should I Go?

Some bacteriophages (viruses that infect bacteria) can undergo a special kind of replication cycle called lysogeny. Rather than making lots of new phages upon infection, these phages can pop their genome into the host chromosome. When the cell copies its DNA and divides, the integrated phage is copied too, so the daughter cells are infected. These integrated phages, or prophages turn out to be very important to us: cholera is caused by V. cholera bacteria with an integrated phage that expresses the toxin that causes diarrhea.
So what is the evolutionary advantage of the lysogenic/lytic switch for this phage? When would it “choose” one over the other? In my biol 105 class we discussed the evolutionary benefits of lysogeny. One of the most enjoyable parts of teaching is when students ask challenging questions that lead to fruitful discussion and deeper thought. Here is my perspective on this.
You can think of the lytic cycle as highly virulent (100% mortality) or lysogenic as non-virulent (no negative effect on the host while the phage is present as a prophage). Virulence is often related to transmission, such that viruses will evolve to have the optimal level of virulence to allow for efficient transmission. Since lysogenic phages can switch between high and low virulence, when would high virulence be favored for transmission and when would low virulence be favored?
A highly virulent pathogen runs the risk of wiping out its host population. If the cells are growing actively in an environment like the gut, and the virus is replicating to high levels, it could spread to the entire host population eventually killing every cell. The virus would then depend on either more V. cholera entering the gut, or getting out of the gut and spreading to a new human host infected with cholera. Alternatively, cholera can also grow in the environment, so the phage could infect a cell in the environment. However there is some obvious risk there, that of finding the next host cholera cell either in a gut or the environment. Its a big world out there for a tiny phage and a tiny bacterial cell to meet each other. A less risky approach might be to limit virulence and allow prophage infected cells to survive. The cholera cells will be returned to the environment, where they can replicate or to a new human host where it can also replicate. Either way, the phage is guaranteed to find a host, because its already in it.
Now if the prophage finds itself in cells that are no longer growing, there may be an advantage to getting out and finding “happy” hosts. Cells that are not growing could be at greater risk of cell damage and death, perhaps they are not acquiring the nutrients and energy necessary to grow or repair cellular damage. If the cell dies, the phage will not be able to replicate. So the phage would enter the lytic cycle and release progeny. The risk of not finding a new host would presumably be lower than the risk of staying within a dying host. High virulence therefore is advantageous for transmission in this situation.
Does anyone have a different perspective?


Distant Evolutionary Relationships

We’ve been talking about protein structure and folding in my Biol 105 class.  Proteins are made of chains of amino acids and the sequence of amino acids, or primary structure, dictates the way the protein will fold into its final 3D or tertiary structure.  We may assume that two proteins with similar sequences would have a similar structure, and that two proteins with very different sequences would have different structures.  However, this is not true.  Proteins with very different sequences can end up with similar 3D structures.

A great example of this is the structure of capsid proteins from three very different viruses.  Adenoviruses infect animals (eukaryotes), and is one of many viruses that cause colds.  PRD1 is a bacteriphage, a virus that infects bacteria.  STIV (Sulfolobus turreted icosahedral virus) infects Sulfolobus, an archaea that lives in geothermal hotsprings in Yellowstone National Park.  STIV and its host love the 80 degree celsius, pH 3 environment of the hotsprings.  The fact that there are viruses that infect archaea in those extreme environments is cool enough.  But it turns out that the capsid proteins of these three viruses are actually quite similar.  Their sequence differs significantly, but their tertiary structures are highly similar, meaning these very different polypeptides fold into essentially the same shape.

What is the basis of this similarity?  Do all theses viruses share a common ancestor, which would have existed before the three domains of cellular life (eukarya, bacteria, archaea) diverged over 3 billion years ago? Is it convergent evolution?  Was there a horizontal gene transfer event in which a gene moved among all three domains?  The authors of the paper argue for a common ancestor but the other possibilities have not been formally excluded.  We still don’t really know, and it raises interesting questions about the origin of viruses.