Rolf Renne,

Rolf Renne, Ph.D., is a Professor in the Department of Molecular Genetics and Microbiology, and has studiesd different aspects of Kaposi’s sarcoma-associated herpesvirus (KSHV) since 1995. His current focus is on epigenetic regulation of viral latency and the role of long and small non-coding RNAs in viral biology. His laboratory is using genomics, genetics, and ribonomics approaches to study how viral-encoded genes and microRNAs contribute to KSHV biology and tumorigenesis.

Dr. Renne received his Master’s (1989) and Ph.D. (1993) degrees from the Albert-Ludwigs University of Freiburg, Germany. He performed most of his Ph.D. thesis work at the University of California Davis with Dr. Paul Luciw in the field of Retrovirology. Next, he joined the laboratory of Dr. Don Ganem, UCSF, where he contributed to early work on establishing tissue culture models for KSHV. In 1999, he joined the faculty at Case Western Reserve University, where he focused on molecular aspects such as DNA binding and DNA replication of the KSHV latency-associated nuclear antigen (LANA) and the establishment of the only available KS xenograft model. In 2004, he moved to the University of Florida, where his laboratory was one of four to identify KSHV-encoded microRNAs. More recently, Dr. Renne has contributed to studies on HSV-1, EBV, HHV-6, MHV-68, and poxviruses. Dr. Renne has been continuously funded by multiple NCI grants since 2004, and in 2017, was awarded a multi-investigator NCI Program project together with Drs. Scott Tibbetts (UF), and Erik Flemington (Tulane University). This P01 Project was successfully renewed in 2022. Dr. Renne is on the editorial board of Journal of Virology, Virology, and serves on multiple NIH special emphasis panels. In 2009, he co-chaired the 11th International Workshop on KSHV and related agents and in 2015 the 40th International Herpesvirus Workshop. The unifying theme of his research projects is to deepen our understanding on how latent gamma-herpesvirus gene products including microRNAs and long noncoding RNAs contribute to viral tumorigenesis. While his focus is on Kaposi’s sarcoma, Primary effusion lymphomas, he also collaborates on EBV-associated cancer, and animal models such as MHV68 and various noninfectious cancers including breast cancer and melanoma. In 2017, he was appointed Associate Director for Basic Science at the UF Health Cancer Center, and in 2019 was named the Henry E. Innes Professor of Cancer Research. In 2021, he was appointed member of the NCI panel A for Cancer Center reviews.

Fun Fact: My dream is to sail around the world one day. The long-term goal of our research is to understand how latency-associated genes of Kaposi’s Sarcoma-associated Herpesvirus (KSHV), including short (microRNAs) and long noncoding RNAs contribute to viral latency and tumorigenesis. KSHV causes Kaposi’s sarcoma and multiple B cell malignancies in immunosuppressed patients. In South Saharan Africa KS is the most prevalent cancer in man. KSHV has been discovered nearly 30 years ago, however to this date we have not been able to develop an efficient therapeutic approach that targets the virus directly. Studying KSHV is complicated by the fact that we have no practical animal models to study pathogenesis. Hence, to decipher the role of virally encoded long and short noncoding RNAs in tumorigenesis, we have created a highly collaborative approach to comparatively study noncoding RNAs in KSHV, Epstein-Barr Virus, the other human gamma-herpesvirus associated with cancer in humans (with Dr. Flemington at Tulane) and MHV-68 a natural Mouse gamma-herpesvirus associated with B cell lymphomas in mice (with Dr. Scott Tibbetts, MGM UF). Using genetics, genomics, proteomics, and ribonomics-based approaches, we have identified a number of pathways and molecular mechanisms of how noncoding RNAs contribute to pathogenesis of all three viruses. The long-term goal is to identify viral RNAs expressed by the virus or host RNAs perturbed by viral infection that represent tumor vulnerabilities and can be therapeutically targeted

0000-0001-7391-8806