Today is

Department of

Molecular Genetics, Biochemistry & Microbiology

Richard Thompson, PhD

Professor of Molecular Genetics, Biochemistry and Microbiology

Research/Clinical Interests

The goal of the Thompson laboratory is to increase our understanding of the molecular mechanisms underlying Herpes Simplex Virus (HSV) latency and reactivation. These studies will lead to new strategies for the treatment and prevention of HSV infection.

Contact Information

Peer Reviewed Publications

Display All

Sawtell, Nancy M; Thompson, Richard L 2014. Herpes simplex virus mutant generation and dual-detection methods for gaining insight into latent/lytic cycles in vivo. Methods in molecular biology (Clifton, N.J.), 1144 , 129-47

Thompson, Richard L; Williams, Robert W; Kotb, Malak; Sawtell, Nancy M 2014. A forward phenotypically driven unbiased genetic analysis of host genes that moderate herpes simplex virus virulence and stromal keratitis in mice. PloS one, 9 3, e92342

Sawtell, Nancy M; Triezenberg, Steven J; Thompson, Richard L 2011. VP16 serine 375 is a critical determinant of herpes simplex virus exit from latency in vivo. Journal of neurovirology, 17 6, 546-51

Thompson, Richard L; Sawtell, Nancy M 2011. The herpes simplex virus type 1 latency associated transcript locus is required for the maintenance of reactivation competent latent infections. Journal of neurovirology, 17 6, 552-8

Thompson, Richard L; Sawtell, Nancy M 2010. Therapeutic implications of new insights into the critical role of VP16 in initiating the earliest stages of HSV reactivation from latency. Future medicinal chemistry, 2 7, 1099-105

Thompson, Richard L; Preston, Chris M; Sawtell, Nancy M 2009. De novo synthesis of VP16 coordinates the exit from HSV latency in vivo. PLoS pathogens, 5 3, e1000352

Sawtell, N M; Thompson, R L; Haas, R L 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. Journal of virology, 80 1, 38-50

Thompson, R L; Sawtell, N M 2006. Evidence that the herpes simplex virus type 1 ICP0 protein does not initiate reactivation from latency in vivo. Journal of virology, 80 22, 10919-30

Sawtell, N M; Thompson, R L 2004. Comparison of herpes simplex virus reactivation in ganglia in vivo and in explants demonstrates quantitative and qualitative differences. Journal of virology, 78 14, 7784-94

Thompson, R L; Shieh, May T; Sawtell, N M 2003. Analysis of herpes simplex virus ICP0 promoter function in sensory neurons during acute infection, establishment of latency, and reactivation in vivo. Journal of virology, 77 22, 12319-30

Sawtell, N M; Thompson, R L; Stanberry, L R; Bernstein, D I 2001. Early intervention with high-dose acyclovir treatment during primary herpes simplex virus infection reduces latency and subsequent reactivation in the nervous system in vivo. The Journal of infectious diseases, 184 8, 964-71

Thompson, R L; Sawtell, N M 2001. Herpes simplex virus type 1 latency-associated transcript gene promotes neuronal survival. Journal of virology, 75 14, 6660-75

Thompson, R L; Sawtell, N M 2000. HSV latency-associated transcript and neuronal apoptosis. Science (New York, N.Y.), 289 5485, 1651

Thompson, R L; Sawtell, N M 2000. Replication of herpes simplex virus type 1 within trigeminal ganglia is required for high frequency but not high viral genome copy number latency. Journal of virology, 74 2, 965-74

Sawtell, N M; Poon, D K; Tansky, C S; Thompson, R L 1998. The latent herpes simplex virus type 1 genome copy number in individual neurons is virus strain specific and correlates with reactivation. Journal of virology, 72 7, 5343-50

Thompson, R L; Sawtell, N M 1997. The herpes simplex virus type 1 latency-associated transcript gene regulates the establishment of latency. Journal of virology, 71 7, 5432-40

Perng, G C; Chokephaibulkit, K; Thompson, R L; Sawtell, N M; Slanina, S M; Ghiasi, H; Nesburn, A B; Wechsler, S L 1996. The region of the herpes simplex virus type 1 LAT gene that is colinear with the ICP34.5 gene is not involved in spontaneous reactivation. Journal of virology, 70 1, 282-91

Perng, G C; Thompson, R L; Sawtell, N M; Taylor, W E; Slanina, S M; Ghiasi, H; Kaiwar, R; Nesburn, A B; Wechsler, S L 1995. An avirulent ICP34.5 deletion mutant of herpes simplex virus type 1 is capable of in vivo spontaneous reactivation. Journal of virology, 69 5, 3033-41

Bolovan, C A; Sawtell, N M; Thompson, R L 1994. ICP34.5 mutants of herpes simplex virus type 1 strain 17syn+ are attenuated for neurovirulence in mice and for replication in confluent primary mouse embryo cell cultures. Journal of virology, 68 1, 48-55

Pyles, R B; Thompson, R L 1994. Evidence that the herpes simplex virus type 1 uracil DNA glycosylase is required for efficient viral replication and latency in the murine nervous system. Journal of virology, 68 8, 4963-72

Pyles, R B; Sawtell, N M; Thompson, R L 1992. Herpes simplex virus type 1 dUTPase mutants are attenuated for neurovirulence, neuroinvasiveness, and reactivation from latency. Journal of virology, 66 11, 6706-13

Sawtell, N M; Thompson, R L 1992. Herpes simplex virus type 1 latency-associated transcription unit promotes anatomical site-dependent establishment and reactivation from latency. Journal of virology, 66 4, 2157-69

Sawtell, N M; Thompson, R L 1992. Rapid in vivo reactivation of herpes simplex virus in latently infected murine ganglionic neurons after transient hyperthermia. Journal of virology, 66 4, 2150-6

Thompson, R L; Rogers, S K; Zerhusen, M A 1989. Herpes simplex virus neurovirulence and productive infection of neural cells is associated with a function which maps between 0.82 and 0.832 map units on the HSV genome. Virology, 172 2, 435-50

Thompson, R L; Devi-Rao, G V; Wagner, E K 1988. DNA sequence and RNA transcription through a site of recombination in a non-neurovirulent herpes simplex virus intertypic recombinant. Virus genes, 1 3, 275-86

Thompson, R L; Wagner, E K 1988. Partial rescue of herpes simplex virus neurovirulence with a 3.2 kb cloned DNA fragment. Virus genes, 1 3, 261-73

Cook, M L; Thompson, R L; Stevens, J G 1986. A herpes simplex virus mutant is temperature sensitive for reactivation from the latent state: evidence for selective restriction in neuronal cells. Virology, 155 1, 293-6

Draper, K G; Devi-Rao, G; Costa, R H; Blair, E D; Thompson, R L; Wagner, E K 1986. Characterization of the genes encoding herpes simplex virus type 1 and type 2 alkaline exonucleases and overlapping proteins. Journal of virology, 57 3, 1023-36

Thompson, R L; Cook, M L; Devi-Rao, G B; Wagner, E K; Stevens, J G 1986. Functional and molecular analyses of the avirulent wild-type herpes simplex virus type 1 strain KOS. Journal of virology, 58 1, 203-11

Thompson, R L; Nakashizuka, M; Stevens, J G 1986. Vaccine potential of a live avirulent herpes simplex virus. Microbial pathogenesis, 1 4, 409-16

Costa, R H; Draper, K G; Devi-Rao, G; Thompson, R L; Wagner, E K 1985. Virus-induced modification of the host cell is required for expression of the bacterial chloramphenicol acetyltransferase gene controlled by a late herpes simplex virus promoter (VP5). Journal of virology, 56 1, 19-30

Thompson, R L; Devi-Rao, G V; Stevens, J G; Wagner, E K 1985. Rescue of a herpes simplex virus type 1 neurovirulence function with a cloned DNA fragment. Journal of virology, 55 2, 504-8

Thompson, R L; Stevens, J G 1983. Biological characterization of a herpes simplex virus intertypic recombinant which is completely and specifically non-neurovirulent. Virology, 131 1, 171-9

Thompson, R L; Stevens, J G 1983. Replication at body temperature selects a neurovirulent herpes simplex virus type 2. Infection and immunity, 41 2, 855-7

Thompson, R L; Wagner, E K; Stevens, J G 1983. Physical location of a herpes simplex virus type-1 gene function(s) specifically associated with a 10 million-fold increase in HSV neurovirulence. Virology, 131 1, 180-92