Draft 4/16

The conclusions that are drawn from these results is that SSV developed an escape mutation whenever a dip in the bacterial population of Sulfolobus was shown. This means that at any of these instances the SSV was able to mutate to again be able to kill Sulfolobus. On the graph when there was more diversity and distribution within the immune systems of Sulfolobus the bacterial cells were significantly less susceptible to SSV infection. The conclusion relating to the Sulfolobus and SSV having a mutualistic relationship is something that I have never seen nor thought about before. The SSV uses host machinery to create and secrete a toxin that kills healthy uninfected cells. The conclusion as to why infected cells are immune to the toxin is that the SSV provides infected cells with an antitoxin keeping them safe. This relationship is considered mutualism because the bacterial cells essentially want to be infected in order to survive. A conclusion about P. aeruginosa infections in humans with chronic CF is that each human is an island population that host the P. aeruginosa and a phage with an anti-CRISPR system which has ways of making CRISPR immunity less effective.