We use high-resolution single-cell and spatial biology approaches to understand how EBV infection rewires host cells and contributes to cancers and autoimmunity
Microbiology & Immunology
Epstein-Barr virus (EBV) infects nearly all adults and poses significant public health burdens worldwide. Discovered in 1964 within cultured Burkitt Lymphoma cells, EBV was the first identified human tumor virus and is now known to be a factor in roughly 2% of all annually diagnosed cancers. In the United States, the most common EBV-associated cancers are B cell lymphomas. The risk of developing such cancers is substantially greater for people living with HIV, transplant recipients taking immunosuppressive therapies, and the elderly. Around the world, other notable EBV-associated cancers include endemic Burkitt Lymphoma, nasopharyngeal carcinoma, and around 10% of gastric carcinomas. EBV is also a causative agent of infectious mononucleosis (IM), a likely essential trigger for onset of multiple sclerosis (MS), and a risk factor for systemic lupus erythematosus (SLE). Despite these diverse associations, the lifelong persistence of the virus, and periodic reactivation from latency to lytic replication, most infected individuals do not experience serious EBV-related diseases. These observations highlight two major points. First, there are still many unanswered questions related to host-pathogen interactions underlying EBV involvement in human diseases. Second, experimental approaches capable of resolving complex and heterogeneous responses of individual cells during EBV infection will be essential to answer those questions.
Our lab applies high-resolution, high-dimensional technologies and computational analyses to study EBV-host dynamics relevant to virus-associated diseases. These include single-cell sequencing (scRNA-seq, scATAC-seq), flow cytometry, and microscopy as well as spatial transcriptomics and in situ hybridization. We leverage these methods in conjunction with experimentally tractable models of infection to define key host-virus regulatory axes and mechanisms by which EBV reprograms host cells to pathogenic states. Through collaborations with clinicians at U-M and beyond, we are also interested in characterizing the genome-wide landscapes of EBV-associated tumors and their microenvironments. Our projects, which are outlined in the Research section, are motivated by the complementary goals of understanding fundamental host-virus genomic regulation in exquisite detail and informing better treatments for EBV-associated diseases.
Please email Dr. Elliott SoRelle (Lab PI) if you’d like to learn more about EBV, our research, or are interested in joining our team.
1137 Catherine St.
Ann Arbor, MI 48109