N M Sawtell

Summary

Affiliation: Children's Hospital Medical Center
Country: USA

Publications

  1. ncbi The probability of in vivo reactivation of herpes simplex virus type 1 increases with the number of latently infected neurons in the ganglia
    N M Sawtell
    Division of Infectious Diseases, Children s Hospital Medical Center, Cincinnati, Ohio 45229 3039, USA
    J Virol 72:6888-92. 1998
  2. ncbi A temporal analysis of acyclovir inhibition of induced herpes simplex virus type 1 In vivo reactivation in the mouse trigeminal ganglia
    N M Sawtell
    Division of Infectious Diseases, Children s Hospital Medical Center, Cincinnati, Ohio 45229 3039, USA
    J Infect Dis 180:821-3. 1999
  3. ncbi Early intervention with high-dose acyclovir treatment during primary herpes simplex virus infection reduces latency and subsequent reactivation in the nervous system in vivo
    N M Sawtell
    Division of Infectious Diseases, Children s Hospital Medical Center, Cincinnati, OH 45229 3039, USA
    J Infect Dis 184:964-71. 2001
  4. ncbi Quantitative analysis of herpes simplex virus reactivation in vivo demonstrates that reactivation in the nervous system is not inhibited at early times postinoculation
    N M Sawtell
    Division of Infectious Diseases, Children s Hospital Medical Center, Cincinnati, Ohio 45229 3039, USA
    J Virol 77:4127-38. 2003
  5. ncbi Comparison of herpes simplex virus reactivation in ganglia in vivo and in explants demonstrates quantitative and qualitative differences
    N M Sawtell
    Division of Infectious Diseases, Children s Hospital Medical Center, Cincinnati, OH 45229 3039, USA
    J Virol 78:7784-94. 2004
  6. ncbi 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
    N M Sawtell
    Division of Infectious Diseases, Cincinnati Children s Hospital Medical Center, 3333 Burnet Ave, Cincinnati, OH 45229 3039, USA
    J Virol 80:38-50. 2006
  7. ncbi Evidence that the herpes simplex virus type 1 ICP0 protein does not initiate reactivation from latency in vivo
    R L Thompson
    Cincinnati Children s Hospital Medical Center, Division of Infectious Diseases, 3333 Burnet Ave, Cincinnati, OH 45229 3039, USA
    J Virol 80:10919-30. 2006
  8. ncbi Herpes simplex virus type 1 latency-associated transcript gene promotes neuronal survival
    R L Thompson
    Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati Medical Center, 231 Albert Sabin Way, Cincinnati, Ohio 45267 0524, USA
    J Virol 75:6660-75. 2001
  9. ncbi Analysis of herpes simplex virus ICP0 promoter function in sensory neurons during acute infection, establishment of latency, and reactivation in vivo
    R L Thompson
    Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267 0524, USA
    J Virol 77:12319-30. 2003
  10. ncbi Preparation of single cells from solid tissues for analysis by PCR
    N M Sawtell
    Children's Hospital Medical Center, Cincinnati, Ohio, USA
    Curr Protoc Mol Biol . 2002

Detail Information

Publications10

  1. ncbi The probability of in vivo reactivation of herpes simplex virus type 1 increases with the number of latently infected neurons in the ganglia
    N M Sawtell
    Division of Infectious Diseases, Children s Hospital Medical Center, Cincinnati, Ohio 45229 3039, USA
    J Virol 72:6888-92. 1998
    ..The number of animals that exhibited virus reactivation was positively correlated with the number of latently infected neurons in the ganglia over the entire range examined (r = 0.9852, P < 0. 0001 [Pearson correlation])...
  2. ncbi A temporal analysis of acyclovir inhibition of induced herpes simplex virus type 1 In vivo reactivation in the mouse trigeminal ganglia
    N M Sawtell
    Division of Infectious Diseases, Children s Hospital Medical Center, Cincinnati, Ohio 45229 3039, USA
    J Infect Dis 180:821-3. 1999
    ..A single dose administered 6-9 h after HS resulted in >90% reduction in reactivation. Acyclovir administered 12 h after HS resulted in 75% reduction, but there was no effect if treatment was delayed for 18 h after HS...
  3. ncbi Early intervention with high-dose acyclovir treatment during primary herpes simplex virus infection reduces latency and subsequent reactivation in the nervous system in vivo
    N M Sawtell
    Division of Infectious Diseases, Children s Hospital Medical Center, Cincinnati, OH 45229 3039, USA
    J Infect Dis 184:964-71. 2001
    ..These findings indicate that potent antiviral therapy during early primary HSV infection can reduce the magnitude of the latent infection, such that a significant decrease in reactivation is observed...
  4. ncbi Quantitative analysis of herpes simplex virus reactivation in vivo demonstrates that reactivation in the nervous system is not inhibited at early times postinoculation
    N M Sawtell
    Division of Infectious Diseases, Children s Hospital Medical Center, Cincinnati, Ohio 45229 3039, USA
    J Virol 77:4127-38. 2003
    ..These data indicate that, in contrast to observations in the ex vivo model, immune cells in the ganglia during the resolution of acute infection do not inhibit reactivation of the virus in ganglia in vivo...
  5. ncbi Comparison of herpes simplex virus reactivation in ganglia in vivo and in explants demonstrates quantitative and qualitative differences
    N M Sawtell
    Division of Infectious Diseases, Children s Hospital Medical Center, Cincinnati, OH 45229 3039, USA
    J Virol 78:7784-94. 2004
    ..This ongoing neurodegeneration could alter even the early virus-host interactions in reactivation, and thus caution in the extrapolation of results obtained in explants to the in vivo interactions initiating reactivation is warranted...
  6. ncbi 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
    N M Sawtell
    Division of Infectious Diseases, Cincinnati Children s Hospital Medical Center, 3333 Burnet Ave, Cincinnati, OH 45229 3039, USA
    J Virol 80:38-50. 2006
    ..We conclude that viral DNA replication in the neuron per se does not regulate IE gene expression or entry into the lytic cycle...
  7. ncbi Evidence that the herpes simplex virus type 1 ICP0 protein does not initiate reactivation from latency in vivo
    R L Thompson
    Cincinnati Children s Hospital Medical Center, Division of Infectious Diseases, 3333 Burnet Ave, Cincinnati, OH 45229 3039, USA
    J Virol 80:10919-30. 2006
    ..We conclude that while ICP0 is important and perhaps essential for infectious virus production during reactivation in vivo, this protein is not required and appears to play no major role in the initiation of reactivation in vivo...
  8. ncbi Herpes simplex virus type 1 latency-associated transcript gene promotes neuronal survival
    R L Thompson
    Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati Medical Center, 231 Albert Sabin Way, Cincinnati, Ohio 45267 0524, USA
    J Virol 75:6660-75. 2001
    ..Thus, one function of the LAT gene is to protect sensory neurons and enhance the establishment of latency in the PNS...
  9. ncbi Analysis of herpes simplex virus ICP0 promoter function in sensory neurons during acute infection, establishment of latency, and reactivation in vivo
    R L Thompson
    Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati Medical Center, Cincinnati, Ohio 45267 0524, USA
    J Virol 77:12319-30. 2003
    ..These last results strongly suggest that there is a posttranscriptional constraint on the expression of ICP0 protein during reactivation from latency and that this constraint is mediated by LAT...
  10. ncbi Preparation of single cells from solid tissues for analysis by PCR
    N M Sawtell
    Children's Hospital Medical Center, Cincinnati, Ohio, USA
    Curr Protoc Mol Biol . 2002
    ..The procedure can also be adapted to allow the quantification of the number of cells within a tissue containing specific nucleic acid sequences, for example, a particular viral DNA or RNA sequence...