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Our lab focuses on understanding the molecular mechanisms underlying herpes simplex virus (HSV) latency and reactivation. These processes are central to the human disease caused by this virus. Our research efforts encompass many approaches, from in vitro biochemical and molecular studies to the development and utilization of refined in vivo model systems.
Recently, we have made an observation that shifts the HSV reactivation paradigm, identifying an essential role for the viral tegument protein VP16 in the earliest stages of HSV reactivation in neurons in vivo.
Several ongoing projects stem from this observation:
Our additional areas of investigation include:
Read more about the Sawtell lab’s herpes simplex research.
Thompson RL, Sawtell NM. Evidence that the herpes simplex virus type 1 ICP0 protein does not initiate reactivation from latency in vivo. J Virol. 80(22): p. 10919-30. 2006.
Sawtell NM, Thompson RL, Haas RL. Herpes simplex virus DNA synthesis is not a decisive regulatory event in the initiation of lytic viral protein expression in neurons in vivo during primary infection or reactivation from latency. J Virol. 80(1): p. 38-50. 2006.
Sawtell NM, Thompson RL. Comparison of herpes simplex virus reactivation in ganglia in vivo and in explants demonstrates quantitative and qualitative differences. J Virol. 78(14): p. 7784-94. 2004.
Sawtell NM. Quantitative analysis of herpes simplex virus reactivation in vivo demonstrates that reactivation in the nervous system is not inhibited at early times postinoculation. J Virol. 77(7): p. 4127-38. 2003.
Thompson RL, Sawtell NM. Herpes simplex virus type 1 latency-associated transcript gene promotes neuronal survival. J Virol. 75(14): p. 6660-75. 2001.
Sawtell NM, et al. Early intervention with high-dose acyclovir treatment during primary herpes simplex virus infection reduces latency and subsequent reactivation in the nervous system in vivo. J Infect Dis. 184(8): p. 964-71. 2001.
Thompson RL, Sawtell NM. Replication of herpes simplex virus type 1 within trigeminal ganglia is required for high frequency but not high viral genome copy number latency. J Virol. 74(2): p. 965-74. 2000.
Thompson RL, Sawtell NM. HSV latency-associated transcript and neuronal apoptosis.Science. 289(5485): p. 1651. 2000.
Sawtell NM. The probability of in vivo reactivation of herpes simplex virus type 1 increases with the number of latently infected neurons in the ganglia. J Virol. 72(8): p. 6888-92. 1998.
Sawtell NM. Comprehensive quantification of herpes simplex virus latency at the single-cell level. J Virol. 71:5423-5431. 1997.
Thompson RL, Sawtell NM. The herpes simplex virus type 1 Latency-Associated Transcript gene regulates the establishment of latency. J Virol. 71:5432-5440. 1997.
Sawtell NM, Thompson RL. Herpes simplex virus type 1 latency-associated transcription unit promotes anatomical site-dependent establishment and reactivation from latency. J Virol. 66:2157-2169. 1992.
Sawtell NM, Thompson RL. Rapid in vivo reactivation of herpes simplex virus in latently infected murine ganglionic neurons after transient hyperthermia. J Virol. 66:2150-2156. 1992.
Nancy Sawtell, PhDDivision of Infectious Diseases3333 Burnet Ave.MLC 7017Cincinnati, OH 45229-3039
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