Prof. Ronit Sarid
Kaposi's sarcoma-associated herpesvirus (KSHV); Human herpesvirus 8 (HHV8); Cancer; latent/lytic infection; Herpes simplex virus (HSV)
CV
Research
Herpesvirus Biology and Pathogenesis
Research in the laboratory focuses on Kaposi’s sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV-8). KSHV is classified as a human tumor virus and is an essential causative agent in the development of Kaposi's sarcoma and certain lymphoproliferative disorders. The classic form of Kaposi's sarcoma has historically shown relatively high incidence rates in Israel. Similar to other herpesviruses, the KSHV genome encodes structural proteins and proteins involved in viral replication, alongside non-coding RNAs and numerous genes that share homology with cellular genes involved in regulating cell cycle progression, cell survival, and signal transduction pathways.
The laboratory investigates the cellular and viral signaling networks that enable productive infection, the establishment of viral latency, and the transition from latency to the lytic cycle. Beyond viral biology itself, the research provides insights into fundamental cellular processes and the roles of host-cell proteins in maintaining the balance between viral infection and normal cellular function. Using genetic manipulation, recombinant viruses, and protein–protein interaction analyses, the research focuses on three main areas:
- Characterizing the roles of viral gene products at different stages of infection, with an emphasis on early stages and the lytic cycle.
- Identifying and characterizing interactions between KSHV-encoded proteins and host-cell proteins and regulatory machinery.
- Mapping cellular proteins and processes specifically regulated during infection to better understand viral biology and associated oncogenic mechanisms.
Courses
- 803204 - Virology
- 80962 - Seminar project for non-thesis graduate students
Publications
Selected Publication
1. Gelgor, A., Kalt, I., Bergson, S., Brulois, K. F., Jung, J. U., & Sarid, R. (2015). Viral Bcl-2 encoded by the Kaposi’s sarcoma-associated herpesvirus is vital for virus reactivation. Journal of Virology, 89(10), 5298–5307.
https://doi.org/10.1128/JVI.00098-15
Demonstrates that the viral protein vBcl-2 is essential for efficient KSHV reactivation and infectious virus production, revealing a critical role in the lytic infection cycle beyond its known functions in regulating cell death and autophagy.
2. Haddad, C. O., Kalt, I., Shovman, Y., Xia, L., Schlesinger, Y., Sarid, R., & Parnas, O. (2021). Targeting the Kaposi’s sarcoma-associated herpesvirus genome with the CRISPR-Cas9 platform in latently infected cells. Virology Journal, 18, 56.
https://doi.org/10.1186/s12985-021-01527-x
Demonstrates that CRISPR-Cas9 can target latent KSHV genomes and reduce viral DNA levels in infected cells, establishing an experimental approach for investigating viral gene function and the mechanisms maintaining persistent infection.
3. Dünn-Kittenplon, D., Ashkenazy-Titelman, A., Kalt, I., Lellouche, J.-P., Shav-Tal, Y., & Sarid, R. (2021). The portal vertex of KSHV promotes docking of capsids at the nuclear pores. Viruses, 13(4), 597.
https://doi.org/10.3390/v13040597
Shows that the KSHV capsid portal promotes efficient docking at nuclear pores, providing insight into how incoming viral particles interact with the nuclear envelope to deliver their genomes into host-cell nuclei
4. Gam ze Letova, C., Kalt, I., Shamay, M., & Sarid, R. (2021). Latently KSHV-infected cells promote further establishment of latency upon superinfection with KSHV. International Journal of Molecular Sciences, 22(21), 11994.
https://doi.org/10.3390/ijms222111994
Reveals that cells already carrying latent KSHV can acquire additional viral genomes and establish latency more efficiently, identifying a role for the viral protein LANA-1 in sustaining persistent infection
5. Atari, N., Rajan, K. S., Chikne, V., Cohen-Chalamish, S., Doniger, T., Orbaum, O., Jacob, A., Kalt, I., Michaeli, S., & Sarid, R. (2022). Lytic reactivation of the Kaposi’s sarcoma-associated herpesvirus (KSHV) is accompanied by major nucleolar alterations. Viruses, 14(8), 1720.
https://doi.org/10.3390/v14081720
Shows that KSHV lytic reactivation causes extensive reorganization of the nucleolus while ribosomal RNA transcription and processing continue, revealing how fundamental cellular processes persist despite major changes in nuclear organization.
6. Orbaum-Harel, O., Sloutskin, A., Kalt, I., & Sarid, R. (2024). KSHV ORF20 promotes coordinated lytic reactivation for increased infectious particle production. Viruses, 16(9), 1418.
https://doi.org/10.3390/v16091418
Demonstrates that the viral protein ORF20 coordinates the progression of KSHV lytic reactivation and supports efficient infectious particle production, identifying a mechanism that helps balance viral replication with host-cell survival.
7. Kalt, I., Ohev, S., Gelgor Dontsov, A., Haddad, C. O., Koren, I., Fuchs, R., Hagai, T., & Sarid, R. (2026). KLHL9 acts as a KSHV vBcl-2-interacting host factor that supports lytic replication. bioRxiv [Preprint].
https://doi.org/10.64898/2026.08.13.744635
Identifies the cellular protein KLHL9 as a binding partner of viral vBcl-2 and shows that KLHL9 supports efficient KSHV lytic replication, revealing a previously uncharacterized virus–host interaction involved in infectious particle production.
Last Updated Date : 15/10/2026
