Humans: Balancing Immunity with Cancer Risk?

 
Viruses utilize many of their host's enzymes and cellular processes in order to multiply and spread infection. In turn, host genes evolve to prevent this from happening. We are interested in understanding how our genes change enough to avoid susceptibility to new viruses, yet still maintain the important functions that they perform in the human body. We are approaching this problem by trying to answer three specific questions regarding the host-virus relationship:

  1. 1) What host genes are being exploited by viruses,

  2. 2) How do viruses cause these host genes to change over time, and

  3. 3) How does this impact the host in the absence of the viral pathogen?


Retroviruses (HIV is a retrovirus) integrate permanently into the genomes of their hosts where they can cause damage from within. This property is devastating, because these integrated copies keep us from ever being able to eradicate HIV from the body of an infected person. Luckily, there is a wonderful model system for this phenomenon. Baker's yeast harbors retrovirus-like Ty elements in its simple genome, and we are using this system to understand the interaction between retroviruses and their hosts at the step of DNA integration. Our hypothesis is that DNA repair genes are being shaped by antagonism from retroviruses and retrotransposons. The implications for this may be that the general process of DNA repair is not as efficient as it could be, potentially contributing to our cancer risk.