Li Lab

DNA repeat sequences in our genome resemble viral DNA, yet the functional significance of these virus-like repeats remains a mystery. Abnormal repeats have also been found at unstable genomic regions implicated in cancer and genetic diseases. Again, how these repeats contribute to genomic instability is poorly understood. Finally, while DNA viruses like Epstein Barr Virus (EBV) have been associated with cancer, it is not clear how exactly these viruses contribute to the development of cancer. For decades, these seemingly disparate yet connected observations pointed towards a missing link between repeat DNA, genomic instability, and viruses.

Our recent discovery of a cluster of EBV-like repeats in our genome provides this missing piece to the puzzle. We showed how virus-like DNA repeats can break and trigger chromosomal abnormalities when bound by a viral protein produced in latent infection. Based on this discovery, our lab will uncover the missing mechanistic link fundamental to the relationship between humans and viruses in health and disease. Currently, we are excited about investigating: 

1. How virus-like DNA repeat sequences undergo breakage
2. How such breakage shapes abnormal genomes that underlie cancer and genetic diseases 
3. Pathological conditions in viral infection that trigger breakage
4. Functional significance of these DNA repeat sequences in normal genome structure and function

Ultimately, we are excited about potentially uncovering a class of viral proteins that may play a role in human health and disease by binding to virus-like repeat sequences in our genome. Understanding these basic mechanisms surrounding virus-like repeats will create new opportunities for the prevention and treatment of viral infection-associated cancer and genetic diseases.

We invite you to learn more about our lab at thejulialilab.com.