Bernadett Papp
University of Florida, FL·Microbiology & Immunology
The mouth is a common entry point for viruses, and it hosts a crowded community of bacteria and fungi whose chemical products bathe the cells lining it. One virus that enters this way is Kaposi's sarcoma-associated herpesvirus (KSHV), a cancer-causing virus linked to Kaposi's sarcoma and to B cell lymphomas in people with AIDS.
- Fields
Microbiology & Immunology
Biochemistry
Genetics
- Topics
Kaposi's sarcoma-associated herpesvirus
lytic reactivation
viral latency
- Grants
- 2 known grants, through Apr 2030
What they work on
- Determine how short-chain fatty acids, small molecules released by oral bacteria, increase protein levels of stress response-related host transcription factors in oral epithelial cells, and how those factors promote KSHV infection.
- Identify KSHV viral factors that can themselves induce stress response-related host transcription factors, and test how important each is for infection of oral epithelial cells.
- Test the hypothesis that KSHV proteins carrying candidate Forkhead-associated (FHA) domain binding motifs, flagged by in silico screening of viral sequences, bind FHA-containing host proteins and alter their cellular functions.
- Dissect one novel viral-FHA protein pair in mechanistic detail and define its role in driving the KSHV lytic cycle, the phase in which the virus replicates and spreads.
- Evaluate whether blocking the identified virus-host interaction can serve as an antiviral approach against KSHV.
More about the research
Like other herpesviruses, KSHV usually settles into a quiet, latent state but can switch into its lytic cycle, in which it copies itself and spreads to new hosts. Two projects here ask how the oral environment and the virus's own proteins tip cells toward supporting that productive, transmissible state, with the practical goal of finding steps a drug could block.
Why it matters
KSHV causes Kaposi's sarcoma and AIDS-related lymphomas and spreads chiefly through the mouth. Identifying the host factors and bacterial metabolites that make oral tissue permissive, and the viral motifs that hijack host proteins, could yield targets for antiviral treatments that interrupt transmission. Because other pathogens use similar tricks, such targets may apply beyond this one virus.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Neelam Sharma-Walia
Rosalind Franklin University of Medicine and Science, IL·Microbiology & Immunology
Determine how KSHV infection turns up the host protein nucleolin and whether nucleolin is needed to keep the virus in its quiet latent state, studying infected endothelial cells and primary effusion lymphoma cells.
David Morgens
Louisiana State University Health Sciences Center-Shreveport, LA·Microbiology & Immunology·Early-career
Identify mutations in KSHV's DNA replication proteins that block late gene expression but still allow viral DNA copying, using a high-throughput method for making and testing many viral mutants.
Allison Didychuk
Yale University, CT·Microbiology & Immunology·Early-career
Determine the function of an essential but poorly understood herpesvirus packaging factor using proteomics and microscopy, and develop deep mutational scanning (testing many mutations at once) for herpesviral proteins.
The school
University of Florida: 65 labs on PI Pages, $1.3B a year on research, 795 research doctorates a year.
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