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Richard Thompson
Richard 
Thompson
, Ph.D.
Professor

B.S. 1971-1975 , University Of Arizona , AK

Ph.D. 1978-83 , University Of California , CA

During acute infection, herpes simplex virus expresses on the order of 80 genes. However, infection of neurons leads to the establishment of a latent infection and only one viral locus is transcribed. Periodic reactivation from latency is the leading infectious cause of blindness, and can result in fatal encephalitis. A major thrust of our laboratory is to identify and characterize viral genes specifically involved in the invasion and destruction of the nervous system, and to explore the molecular mechanisms of the establishment of, and reactivation from, the latent state.

We have developed a model system in which all facets of human disease can be examined, including the establishment of latent infections, and rapid induction of reactivation with a physiologically relevant procedure. Currently, a variety of recombinant DNA and genetic engineering techniques are being employed to determine the factors which regulate the expression of key viral genes in specific cell types. Parallel experiments are designed to investigate the structural chemistry and function of the proteins encoded by these genes. Results to date suggest it will be possible to define precisely the pathobiology of HSV on a molecular level, to design new strategies for the prevention and treatment of herpetic disease, and to exploit viral properties to generate gene transfer vectors for the nervous system

Selected Publications:
  • Thompson RL, Preston CM, and Sawtell NM. (2009) De novo synthesis of VP16 coordinates the exit from HSV latency in vivo. PLoS Pathog, March, 5(3): e1000352.
  • Sawtell NM, Thompson RL, and Haas RL. (2006) 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):38-50.
  • Thompson RL and Sawtell NM. (2006) Evidence that the Herpes Simplex Virus Type 1 ICP0 Protein Does Not Initiate Reactivation from Latency In Vivo. J Virol. 80(22):10919-30.
  • Sawtell NM and Thompson RL. (2004) Comparison of herpes simplex virus reactivation in ganglia in vivo and in explants demonstrates quantitative and qualitative differences. J Virol. 78(14):7784-94.
  • Thompson RL, Shieh MT, and Sawtell NM. (2003) Analysis of herpes simplex virus ICP0 promoter function in sensory neurons during acute infection, establishment of latency, and reactivation in vivo. J Virol. 77(22):12319-30.

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