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David A. Leib, PhD

Chair and Professor of Microbiology and Immunology

Additional Titles/Positions/Affiliations
Adjunct Professor of Biology

Microbiology and Immunology

David Leib received his BSc from The University of Birmingham, UK in 1983 in Biological Sciences. He then received his PhD from The University of Liverpool, UK in 1986 from the Department of Medical Microbiology. He did a postdoctoral fellowship at Harvard University with Dr Priscilla Schaffer from 1987-1990. He was then was appointed to the faculty of Washington University in St Louis where he served as Professor until 2009, before moving to Dartmouth. He became Chair of Microbiology and Immunology in 2018.

Immunology Program
Molecular and Cellular Biology Graduate Programs
Molecular Pathogenesis Program

Websites Visit the Leib Lab Website at:


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Contact Information

Geisel School of Medicine at Dartmouth
One Medical Center Drive
Borwell Building 630E
Lebanon NH 03756

Office: 603-650-8616
Fax: 603-650-6223
Email: david.a.leib@dartmouth.edu

Professional Interests

Since its establishment in 1990 my laboratory has studied the pathogenesis and biology of herpes simplex virus (HSV) with an emphasis on studying the interface of the virus and the host. The generation and use of recombinant viruses in a variety of models of infection followed by analysis with functional genomics and cytokine arrays has allowed us to determine the roles of viral and host factors in the outcome of infection. We have developed a number of reagents, techniques, and approaches. These include BACs to rapidly generate recombinant viruses, non-invasive bioluminescence technology to monitor spread and tropism of HSV in real time, and recombinant viruses that are effective as therapeutic vaccines for prevention of recurrent HSV infections (US Patent #5698431). We have also discovered roles for a number of viral genes in the evasion of innate and adaptive immunity, and of autophagy responses, and elucidated roles for host resistance pathways in the control of acute infection.

Herpes simplex virus is a common ocular pathogen causing a variety of diseases ranging from self-limiting dendritic epithelial keratitis, conjunctivitis, and blepharitis to necrotizing stromal keratitis. HSV exhibits two different modes of gene expression during its life cycle. During the replicative phase of infection all of its genes are expressed. During latency, however, viral gene expression is almost completely repressed. Our approach is to manipulate cloned viral genes and then introduce engineered 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.

The ability of HSV to evade innate immunity is critical to its success as a pathogen. A number of projects in the lab are focused on the molecular basis of immune evasion and determining the precise genes and domains that are involved. In particular, we are studying the g34.5 of HSV which has multiple cellular binding partners that collectively serve to control the interferon response, global translation rates, autophagy, mitochondrial function, and egress from the cell. g34.5 is therefore a highly versatile and potent determinant of virulence.

Neonatal herpes simplex virus (nHSV) infections cause devastating morbidity and mortality in infants. Most nHSV cases are associated with primary maternal infection, consistent with the hypothesis that maternal immunity is protective. Our studies show that nHSV can be prevented through maternal vaccination and through administration of therapeutic antibodies whereby protection is passed from the maternal to the fetal circulation. Protection is not only at the level of prevention of virus-induced mortality, but also at the level of prevention of the common neurological complications of nHSV. Through development of behavioral and memory testing we are showing an important connection between HSV infections and behavioral morbidities that may have huge importance in the clinical setting. Permanent behavioral changes may be caused by nHSV in babies born to mothers without preexisting immunity. The maternal virome is therefore likely an important determinant of human health.

Grant Information

Principal Investigator, NEI RO1 09083 "Viral and host factors in herpetic reactivation", Funded 1992-2021.

Principal investigator, NIAID R21 147714 “Monoclonal antibody therapy for neonatal HSV infections
” 2019-2021.

Director, Project 3, AI098681 “Innate immunity and the HSV lytic/latent balance”. Program Project (D.M. Coen, Harvard Medical School, Director)
NIH NIAID PO1 “Viral and host mechanisms that tilt the HSV lytic/latent balance”. Funded 2013-2018.

Courses Taught

Microbiology (BIO46 undergraduate), Fundamentals of Virology.


1983 BSc University of Birmingham (UK).
1986 PhD University of Liverpool (UK).
1987-1990 Postdoctoral fellowship, Harvard University.
1990-2009 Washington University.
2009-Present, Geisel School of Medicine at Dartmouth.

Selected Publications


Models of Herpes Simplex Virus Latency.
Canova PN, Charron AJ, Leib DA
Viruses. 2024 May 8;16(5) doi: 10.3390/v16050747. Epub 2024 May 8.
PMID: 38793628

Asymptomatic neonatal herpes simplex virus infection in mice leads to long-term cognitive impairment.
Dutton A, Patel CD, Taylor SA, Garland CR, Turnbaugh EM, Alers-Velazquez R, Mehrbach J, Nautiyal KM, Leib DA
bioRxiv. 2024 Apr 22; pii: 2024.04.22.590596. doi: 10.1101/2024.04.22.590596. Epub 2024 Apr 22.
PMID: 38712140

Effector functions are required for broad and potent protection of neonatal mice with antibodies targeting HSV glycoprotein D.
Slein MD, Backes IM, Garland CR, Kelkar NS, Leib DA, Ackerman ME
Cell Rep Med. 2024 Feb 20;5(2):101417. doi: 10.1016/j.xcrm.2024.101417. Epub 2024 Feb 12.
PMID: 38350452

Antibody effector functions are required for broad and potent protection of neonates from herpes simplex virus infection.
Slein MD, Backes IM, Garland CR, Kelkar NS, Leib DA, Ackerman ME
bioRxiv. 2023 Aug 31; pii: 2023.08.29.555423. doi: 10.1101/2023.08.29.555423. Epub 2023 Aug 31.
PMID: 37693377

Maternally transferred mAbs protect neonatal mice from HSV-induced mortality and morbidity.
Backes IM, Byrd BK, Slein MD, Patel CD, Taylor SA, Garland CR, MacDonald SW, Balazs AB, Davis SC, Ackerman ME, Leib DA
J Exp Med. 2022 Dec 5;219(12) doi: 10.1084/jem.20220110. Epub 2022 Sep 26.
PMID: 36156707

Monoclonal antibody therapy of herpes simplex virus: An opportunity to decrease congenital and perinatal infections.
Backes IM, Leib DA, Ackerman ME
Front Immunol. 2022;13:959603. doi: 10.3389/fimmu.2022.959603. Epub 2022 Aug 9.
PMID: 36016956

Herpes Simplex Virus-2 Variation Contributes to Neurovirulence During Neonatal Infection.
Hayes CK, Villota CK, McEnany FB, Ceron S, Awasthi S, Szpara ML, Friedman HM, Leib DA, Longnecker R, Weitzman MD, Akhtar LN
J Infect Dis. 2022 Nov 1;226(9):1499-1509. doi: 10.1093/infdis/jiac151.
PMID: 35451492

Herpes Simplex Virus 1 ICP34.5 Alters Mitochondrial Dynamics in Neurons.
Manivanh R, Mehrbach J, Charron AJ, Grassetti A, Ceron S, Taylor SA, Cabrera JR, Gerber S, Leib DA
J Virol. 2020 Jul 1;94(14) doi: 10.1128/JVI.01784-19. Epub 2020 Jul 1.
PMID: 32376626

Trivalent Glycoprotein Subunit Vaccine Prevents Neonatal Herpes Simplex Virus Mortality and Morbidity.
Patel CD, Taylor SA, Mehrbach J, Awasthi S, Friedman HM, Leib DA
J Virol. 2020 May 18;94(11) doi: 10.1128/JVI.02163-19. Epub 2020 May 18.
PMID: 32188735

Maternal immunization confers protection against neonatal herpes simplex mortality and behavioral morbidity.
Patel CD, Backes IM, Taylor SA, Jiang Y, Marchant A, Pesola JM, Coen DM, Knipe DM, Ackerman ME, Leib DA
Sci Transl Med. 2019 Apr 10;11(487) doi: 10.1126/scitranslmed.aau6039.
PMID: 30971454

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