Leib Laboratory

Research

Herpes simplex virus (HSV) is a highly evolved and successful pathogen with a very wide distribution in the human population, close to 100% in some populations. HSV often manages to forge the near-perfect lifelong relationship with us, its human host. Despite the availability of excellent antiviral drugs such as acyclovir and valtrex, HSV is refractory to cure. This is due to the ability of HSV to invade neurons, to translocate to neuronal cell bodies, and establish latent infections therein. Our over-arching interest is to understand how HSV modulates the immune system of the host. This immune-modulation allows HSV to successfully establish latency, and more remarkably, to allow the virus to escape from the immune host to infect other susceptible individuals in the population. Our experimental approach is to use forward and reverse genetics to introduce mutations into the viral genome to generate recombinant viruses. We then use these recombinant viruses in vitro and in vivo to allow the study of viral pathogenesis at the molecular level, and to examine the outcome of the host-pathogen battle.

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Recent Publications

Neuronal subtype determines HSV-1 Latency-Associated-Transcript (LAT) promoter activity during latency.
Cabrera JR, Charron AJ, Leib DA
J Virol. 2018 Apr 11; pii: JVI.00430-18. doi: 10.1128/JVI.00430-18. Epub 2018 Apr 11.
PMID: 29643250

Preventing neonatal herpes infections through maternal immunization.
Jiang Y, Leib D
Future Virol. 2017 Dec;12(12):709-711. doi: 10.2217/fvl-2017-0105.
PMID: 29339967

Role of Herpes Simplex Virus 1 γ34.5 in the Regulation of IRF3 Signaling.
Manivanh R, Mehrbach J, Knipe DM, Leib DA
J Virol. 2017 Dec 1;91(23) pii: e01156-17. doi: 10.1128/JVI.01156-17. Epub 2017 Nov 14.
PMID: 28904192

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