Our scientific question is how viruses promote cancer development
The research interests in the lab are to study the functional interactions between viral proteins and the cellular machinery, which control both the viral life cycle and tumorigenesis. About 15% of the cancers in humans are associated with viral infections. The viruses we study are the human gamma herpes viruses; Kaposi’s sarcoma associated herpesvirus (KSHV, HHV-8) and Epstein-Barr virus (EBV, HHV-4) that are associated with increasing number of human malignancies. EBV is a ubiquitous virus that infects over 90% of adults worldwide, including Israel. KSHV prevalence varies significantly depending on the geographic regions; in Israel about 10% are infected. While in the majority of infected individuals these viruses do not lead to cancer development, under specific condition such as suppression of the immune system they promote cancer development. The goal of our lab is to expand our knowledge on viral infections, and to utilize this knowledge for the development and use of drugs that specifically target virally infected cells.
We have specific interest to understand how these viruses modulate our epigenome. Epigenetic marks such as DNA methylation, histone modifications and chromatin remodeling are important regulators of gene expression. Together with genetic alterations, epigenetic modifications are responsible for the development of many diseases, including cancer. We perform gene specific and whole genome DNA methylation analysis, and combine these with whole transcriptome (RNA-seq) analysis to reveal the impact of viral infection on DNA methylation and gene expression.
Human endogenous viral elements (EVE) or transposable elements (TEs), as their name suggest, have the ability to transpose (jump) within their host genome. They are ubiquitous in eukaryotic genomes, occupying about 45% of the human genome. Our recent study revealed that KSHV infection dysregulate many transposable elements within the infected cells.
Examples of scientific questions we ask:
What are the global epigenetic changes these viruses impose on infected cells during tumor development?
Which epigenetic marks differentiate infected cell from infected cell that become cancerous? The results of these studies will help us to develop novel methods for the detection of viral associated malignancies.
How exogenous virus like KSHV modulates the expression of human endogenous viruses (transposable elements)?
After reading the above, if you have a scientific question related to our study let’s talk about your next project.