Biography

Ronit Sarid is a Full Professor in the Faculty of Life Sciences at Bar-Ilan University, where she has served as the Rector's Advisor for the Advancement of Women in Academia and as the Dean of Graduate Studies. She received her PhD in Virology from Tel Aviv University. During her postdoctoral training at Tel Aviv University and subsequently at Columbia University (New York), she specialized in herpesvirus biology, focusing specifically on Kaposi’s sarcoma-associated herpesvirus (KSHV).

As KSHV is one of the few viruses definitively linked to human oncogenesis, Professor Sarid has been actively engaged in studying its biology virtually since its discovery. While investigating KSHV is critical from clinical and public health standpoints, her work also provides fundamental insights into how viruses drive cellular proliferation and transformation. Currently, her research group focuses on the cellular and viral pathways involved in KSHV infection, with a particular emphasis on the mechanisms governing the lytic cycle.

Research Overview

Kaposi’s sarcoma-associated herpesvirus (KSHV), also designated as human herpesvirus-8 (HHV-8), is one of the few viruses proven to be associated with tumorigenesis in humans. It is causally linked to all clinical and epidemiological variants of Kaposi’s sarcoma (KS), a complex, multifocal neoplasm characterized by the proliferation of spindle-like cells and significant inflammation. KS develops relatively frequently in HIV/AIDS patients and represents the most common cancer in several regions of Africa. It also presents a risk to transplant recipients in endemic areas. Notably, Israel exhibits one of the highest incidence rates of classic KS (primarily affecting elderly men) in the developed world, corresponding with a relatively high KSHV seroprevalence of 10–13% in the Jewish Israeli population. KSHV is also the causative agent behind two lymphoproliferative malignancies: primary effusion lymphoma (PEL) and a subset of multicentric Castleman’s disease (MCD). Beyond its clinical urgency, KSHV serves as an invaluable model for dissecting how viruses manipulate cellular signaling, offering broader clues into normal and tumorigenic signal transduction pathways.

Like all other herpesviruses, primary KSHV infection establishes a lifelong latent state with the persistent potential for lytic reactivation, which drives disease progression. The host factors and signal transduction cascades regulating KSHV infection, lytic reactivation, and an efficient productive cycle remain incompletely understood.

Exploring Cellular and Viral Pathways in the KSHV Lifecycle and Pathogenesis

The Sarid laboratory previously conducted extensive clinical and epidemiological studies to determine the seroprevalence and transmission routes of KSHV within the Israeli population, identify unique clinical presentations associated with infection, characterize viral kinetics during organ transplantation, and evaluate specific biological correlates serving as markers for disease progression. On a molecular level, her reseach was also central to identifying the viral Bcl-2 homolog within the KSHV genome, deciphering key KSHV latent genes, mapping signaling pathways involved in lytic reactivation, and performing foundational functional studies on selected viral proteins.

Currently, the laboratory investigates the cellular and viral signaling networks that facilitate productive infection, support long-term latency, and trigger the switch from latent to lytic replication. By utilizing recombinant KSHV genomes, analyzing viral gene expression, mapping viral-host protein-protein interactions, and examining the functions of selected viral proteins alongside their viral and cellular partners, the lab characterizes the function and regulation of specific viral genes and their protein products. Uncovering the precise functions of these viral proteins clarifies the specific cellular pathways disrupted in KSHV-infected cells and advances our broader understanding of viral biology.