Vera Tarakanova, PhD
Microbiology and Molecular Genetics
Medical College of Wisconsin
Research Focus: Virus-associated Tumorigenesis, Virus-host Interactions
PhD: Saint Louis University, Microbiology
My long-standing interest is the understanding of virus pathobiology that contributes to tumorigenesis. Viruses are thought to play a role in the development of at least 20% of all cancers worldwide, and virus-associated cancers represent a majority of liver and cervical neoplasms. Evolutionary, tumorigenesis is likely an unintended outcome of the viral infection. In the course of viral replication, most so called “tumor” viruses tap into host pathways that, when perturbed, contribute to cellular transformation. Activation and modulation of such host signaling pathways is normally used by the virus to enhance its replication or persistence. However, viral modulation of the same pathways in an immunocompromised host, or in cells where the viral life cycle cannot be completed may lead to the unintended outcome of cellular transformation. Studies of viral interactions with cellular pathways that contribute to transformation will enhance our understanding of both viral biology and virus-associated tumorigenesis.
In my laboratory we use mouse gammaherpesvirus-68 as a model to study virus-host interactions in the context of a tumor-associated virus. This virus is genetically and biologically related to human gammaherpesviruses Epstein-Barr virus and Kaposi’s Sarcoma associated herpesvirus. The ability to genetically manipulate both the virus (murine gammaherpesvirus-68) and the host (laboratory mouse) makes this a highly tractable system to study host and virus factors involved in chronic infection and pathogenesis.
DNA damage signaling is a host network of protein-protein interactions and modifications responsible for detection and resolution of lesions in host DNA. This signaling network is frequently perturbed in most cancers and is modulated by the “tumor” viruses, including mouse gammaherpesvirus-68. A major research goal of my laboratory is to understand how the viral modulation of host DNA damage signaling contributes to long term infection and pathogenesis of this tumor-associated virus.
A. Normal mouse spleen. B. Lymphoma bearing spleen from an immunocompromised mouse infected with murine gammaherpesvirus-68. Note the concise, dark-staining area of white pulp (outlined) in the normal spleen (A). White pulp undergoes massive expansion and becomes filled with homogenous, lightly staining mass of malignant cells in B. Magnification: A, B x40.
Room: MEB BSB-250