معرفی
Kavi Mehta is an Assistant Professor at the University of Wisconsin–Madison, jointly affiliated with the Department of Medical Microbiology and Immunology and the Department of Bacteriology within the School of Medicine and Public Health. His research program focuses on understanding the molecular mechanisms of DNA damage, replication stress, and mutagenesis, particularly in the context of viral infections like human papillomavirus (HPV) and herpesviruses.
His research interests include:
- Strand-specific replication stress responses in mammalian cells
- Mechanisms of mutagenesis due to endogenous and exogenous DNA damage
- How viruses such as HPV alter host replication and DNA repair pathways
- Role of proteins like HMCES and PRIMPOL in maintaining genome integrity
- Transcription-replication conflicts and their resolution
The recent publications from the Mehta Lab reveal a strong trend in understanding how oxidative stress, viral infections, and chemical agents induce DNA damage and genomic instability. Key themes include the role of APOBEC enzymes, abasic site repair, replication fork protection, and viral manipulation of host repair machinery. Much of this work employs cutting-edge molecular biology techniques in human and mammalian cell models.
Scientific contributions include high-impact publications in journals such as Cell, Nature Communications, Science Advances, and Molecular Cell. His work frequently involves collaboration with leading labs, particularly the Cortez and Laimins groups.
Kavi Mehta actively mentors students and researchers in his lab, though specific advisee names are not listed in the provided texts. His lab receives funding to support research on DNA repair, viral oncogenesis, and replication stress. The lab has published on diverse topics including HPV life cycle regulation, herpesvirus replication mechanisms, obesity-related DNA damage, and novel papillomavirus discovery in wildlife.
The Mehta Lab operates at the intersection of molecular virology, DNA repair, and cancer biology, with a strong emphasis on mechanistic insights into genome maintenance under stress. Ongoing projects include investigating leading vs lagging strand stress responses, strand-specific mutagenesis, and how small DNA tumor viruses exploit host replication machinery.
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