David A Thorley-Lawson

Summary

Affiliation: Tufts University
Country: USA

Publications

  1. pmc Peripheral B cells latently infected with Epstein-Barr virus display molecular hallmarks of classical antigen-selected memory B cells
    Tatyana A Souza
    Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA
    Proc Natl Acad Sci U S A 102:18093-8. 2005
  2. pmc Chemotaxis in densely populated tissue determines germinal center anatomy and cell motility: a new paradigm for the development of complex tissues
    Jared B Hawkins
    Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, United States of America
    PLoS ONE 6:e27650. 2011
  3. pmc A novel persistence associated EBV miRNA expression profile is disrupted in neoplasia
    Jin Qiu
    Dept of Pathology, Tufts University School of Medicine, Boston, Massachusetts, United States of America
    PLoS Pathog 7:e1002193. 2011
  4. pmc The pathogenesis of Epstein-Barr virus persistent infection
    David A Thorley-Lawson
    Department of Pathology, Tufts University School of Medicine, Jaharis Building, Boston, MA 02111, USA
    Curr Opin Virol 3:227-32. 2013
  5. ncbi request reprint Epstein-Barr virus: exploiting the immune system
    D A Thorley-Lawson
    Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
    Nat Rev Immunol 1:75-82. 2001
  6. ncbi request reprint Persistence of the Epstein-Barr virus and the origins of associated lymphomas
    David A Thorley-Lawson
    Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA
    N Engl J Med 350:1328-37. 2004
  7. ncbi request reprint EBV the prototypical human tumor virus--just how bad is it?
    David A Thorley-Lawson
    Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA
    J Allergy Clin Immunol 116:251-61; quiz 262. 2005
  8. doi request reprint Epstein-Barr virus: a paradigm for persistent infection - for real and in virtual reality
    David A Thorley-Lawson
    Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
    Trends Immunol 29:195-201. 2008
  9. ncbi request reprint Influence of EBV on the peripheral blood memory B cell compartment
    Tatyana A Souza
    Department of Pathology, Jaharis Building, Tufts University School of Medicine, 150 Harrison Avenue, Boston, MA 02111, USA
    J Immunol 179:3153-60. 2007
  10. pmc Comprehensive profiling of Epstein-Barr virus microRNAs in nasopharyngeal carcinoma
    Katherine Cosmopoulos
    Department of Pathology, Tufts University School of Medicine, Jaharis Building, Boston, Massachusetts 02111, USA
    J Virol 83:2357-67. 2009

Research Grants

  1. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2001
  2. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2002
  3. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 1999
  4. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2003
  5. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2003
  6. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2000
  7. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2006
  8. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2006
  9. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2002
  10. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2004

Collaborators

Detail Information

Publications31

  1. pmc Peripheral B cells latently infected with Epstein-Barr virus display molecular hallmarks of classical antigen-selected memory B cells
    Tatyana A Souza
    Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA
    Proc Natl Acad Sci U S A 102:18093-8. 2005
    ..This article provides definitive evidence that EBV in the peripheral blood persists in true memory B cells...
  2. pmc Chemotaxis in densely populated tissue determines germinal center anatomy and cell motility: a new paradigm for the development of complex tissues
    Jared B Hawkins
    Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, United States of America
    PLoS ONE 6:e27650. 2011
    ..This mechanism may have wide application for modeling other biological systems where cells undergo complex patterns of movement to produce defined anatomical structures with sharp tissue boundaries...
  3. pmc A novel persistence associated EBV miRNA expression profile is disrupted in neoplasia
    Jin Qiu
    Dept of Pathology, Tufts University School of Medicine, Boston, Massachusetts, United States of America
    PLoS Pathog 7:e1002193. 2011
    ..Biologically, this may be a consequence of functional redundancy between the miRNAs...
  4. pmc The pathogenesis of Epstein-Barr virus persistent infection
    David A Thorley-Lawson
    Department of Pathology, Tufts University School of Medicine, Jaharis Building, Boston, MA 02111, USA
    Curr Opin Virol 3:227-32. 2013
    ..Rather, it is the cycle of infection which allows viral persistence at the very low levels observed. ..
  5. ncbi request reprint Epstein-Barr virus: exploiting the immune system
    D A Thorley-Lawson
    Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
    Nat Rev Immunol 1:75-82. 2001
    ....
  6. ncbi request reprint Persistence of the Epstein-Barr virus and the origins of associated lymphomas
    David A Thorley-Lawson
    Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA
    N Engl J Med 350:1328-37. 2004
  7. ncbi request reprint EBV the prototypical human tumor virus--just how bad is it?
    David A Thorley-Lawson
    Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA
    J Allergy Clin Immunol 116:251-61; quiz 262. 2005
    ....
  8. doi request reprint Epstein-Barr virus: a paradigm for persistent infection - for real and in virtual reality
    David A Thorley-Lawson
    Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
    Trends Immunol 29:195-201. 2008
    ....
  9. ncbi request reprint Influence of EBV on the peripheral blood memory B cell compartment
    Tatyana A Souza
    Department of Pathology, Jaharis Building, Tufts University School of Medicine, 150 Harrison Avenue, Boston, MA 02111, USA
    J Immunol 179:3153-60. 2007
    ..These results indicate that EBV impacts the mutation and selection process of infected cells but that once they enter memory they cannot be distinguished from uninfected cells by host homeostasis mechanisms...
  10. pmc Comprehensive profiling of Epstein-Barr virus microRNAs in nasopharyngeal carcinoma
    Katherine Cosmopoulos
    Department of Pathology, Tufts University School of Medicine, Jaharis Building, Boston, Massachusetts 02111, USA
    J Virol 83:2357-67. 2009
    ..However, we confirm the hypothesis that the BHRF1 miRNAs are not expressed in NPC. Lastly, we demonstrate that EBV miRNA expression in the widely used NPC line C666-1 is, with some caveats, broadly representative of primary NPC tumors...
  11. pmc Plasma cell-specific transcription factor XBP-1s binds to and transactivates the Epstein-Barr virus BZLF1 promoter
    Chia Chi Sun
    Department of Pathology, Jaharis Building, Tufts University School of Medicine, 150 Harrison Ave, Boston, MA 02111, USA
    J Virol 81:13566-77. 2007
    ..We are currently investigating other signals, such as the endoplasmic reticulum stress response proteins, which act upstream of XBP-1s, to identify other interacting factors that initiate and/or amplify the lytic switch...
  12. pmc Germinal center B cells latently infected with Epstein-Barr virus proliferate extensively but do not increase in number
    Jill E Roughan
    Dept of Pathology, Jaharis Building, Tufts University School of Medicine, 150 Harrison Ave, Boston, MA 02111, USA
    J Virol 84:1158-68. 2010
    ..This emphasizes our claim that observations made regarding the functions of EBV proteins in cell lines or in transgenic mice should be treated with skepticism unless verified in vivo...
  13. ncbi request reprint IFN-alpha-stimulated genes and Epstein-Barr virus gene expression distinguish WHO type II and III nasopharyngeal carcinomas
    D Michiel Pegtel
    Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA, and Graduate Institute of Microbiology, Department of Otolaryngology, National Taiwan University Hospital, Taipei, Taiwan
    Cancer Res 67:474-81. 2007
    ....
  14. pmc Acute infection with Epstein-Barr virus targets and overwhelms the peripheral memory B-cell compartment with resting, latently infected cells
    Donna Hochberg
    Department of Pathology, Jaharis Building, Tufts University School of Medicine, 150 Harrison Avenue, Boston, MA 02111, USA
    J Virol 78:5194-204. 2004
    ..This phase is followed by a slower decline that, even by 1 year, had not reached a steady state. Therefore, EBV may approach but never reach a stable equilibrium...
  15. pmc Terminal differentiation into plasma cells initiates the replicative cycle of Epstein-Barr virus in vivo
    Lauri L Laichalk
    Dept of Pathology, Jaharis Building, Tufts University School of Medicine, 150 Harrison Ave, Boston, MA 02111, USA
    J Virol 79:1296-307. 2005
    ....
  16. pmc On the dynamics of acute EBV infection and the pathogenesis of infectious mononucleosis
    Vey Hadinoto
    Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA
    Blood 111:1420-7. 2008
    ..The release of antigens caused by this large-scale destruction of infected cells may trigger the symptoms of AIM and be a cofactor in other AIM-associated diseases...
  17. pmc The dynamics of EBV shedding implicate a central role for epithelial cells in amplifying viral output
    Vey Hadinoto
    Department of Pathology, Tufts University School of Medicine, Boston, MA, USA
    PLoS Pathog 5:e1000496. 2009
    ..We suggest that the final size of these plaques is a function of the rate of infectious spread within the lymphoepithelium which may be governed by the structural complexity of the tissue but is ultimately limited by the immune response...
  18. pmc Epstein-Barr-virus-encoded LMP2A induces primary epithelial cell migration and invasion: possible role in nasopharyngeal carcinoma metastasis
    Dirk M Pegtel
    Department of Pathology, Tufts University School of Medicine, Jaharis Building, 150 Harrison Ave, Boston, MA 02111, USA
    J Virol 79:15430-42. 2005
    ..Our results provide a link between LMP2A expression, ITGalpha6 expression, epithelial cell migration, and NPC metastasis and suggest that EBV infection may contribute to the high incidence of metastasis in NPC progression...
  19. ncbi request reprint EBV and systemic lupus erythematosus: a new perspective
    Andrew J Gross
    Division of Rheumatology, Tufts New England Medical Center, Tufts University School of Medicine, Boston, MA 02111, USA
    J Immunol 174:6599-607. 2005
    ..We conclude that the abnormal regulation of EBV infection in SLE patients reflects the sensitivity of the virus to perturbation of the immune system...
  20. pmc Persistence of Epstein-Barr virus in self-reactive memory B cells
    Sean I Tracy
    Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts, USA
    J Virol 86:12330-40. 2012
    ..We suggest that this might reflect an active process where EBV and its human host have coevolved so as to minimize the virus's potential to contribute to autoimmune disease...
  21. pmc Demonstration of the Burkitt's lymphoma Epstein-Barr virus phenotype in dividing latently infected memory cells in vivo
    Donna Hochberg
    Department of Pathology, Tufts University School of Medicine, Jaharis Building, 150 Harrison Avenue, Boston, MA 02111, USA
    Proc Natl Acad Sci U S A 101:239-44. 2004
    ..It suggests that BL may be a tumor of a latently infected memory B cell that is stuck proliferating because it is a tumor and, therefore, constitutively expressing only EBNA1...
  22. pmc Epstein-Barr virus infection in ex vivo tonsil epithelial cell cultures of asymptomatic carriers
    Dirk M Pegtel
    Department of Pathology, Tufts University School of Medicine, Jaharis Bldg, 150 Harrison Avenue, Boston, MA 02111, USA
    J Virol 78:12613-24. 2004
    ..This provides an explanation for the presence of EBV in naso- and oropharyngeal pathologies and is consistent with epithelial cells playing a role in the egress of EBV during persistent infection...
  23. pmc The intersection of Epstein-Barr virus with the germinal center
    Jill E Roughan
    Department of Pathology, Jaharis Building, Tufts University School of Medicine, 150 Harrison Ave, Boston, MA 02111, USA
    J Virol 83:3968-76. 2009
    ..Furthermore, it identifies latently infected GC B cells as a potential pathogenic nexus for the development of the EBV-positive, GC-associated lymphomas Hodgkin's disease and Burkitt's lymphoma...
  24. ncbi request reprint The dispersal of mucosal memory B cells: evidence from persistent EBV infection
    Lauri L Laichalk
    Department of Pathology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA
    Immunity 16:745-54. 2002
    ..This pathway may reflect that of normal memory B cells derived from nasopharyngeal and other mucosal lymph nodes...
  25. ncbi request reprint Quantitative detection of viral gene expression in populations of Epstein-Barr virus-infected cells in vivo
    Donna R Hochberg
    Department of Pathology, Tufts University School of Medicine, Boston, MA, USA
    Methods Mol Biol 292:39-56. 2005
    ..However, this technique can be applied to other cell populations, such as B cells, and other patient groups, such as healthy long-term virus carriers and immunosuppressed organ transplant recipients...
  26. pmc The cycle of EBV infection explains persistence, the sizes of the infected cell populations and which come under CTL regulation
    Jared B Hawkins
    Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America
    PLoS Pathog 9:e1003685. 2013
    ....
  27. doi request reprint The curious case of the tumour virus: 50 years of Burkitt's lymphoma
    David A Thorley-Lawson
    Department of Pathology, Jaharis Building, Tufts University School of Medicine, 150 Harrison Avenue, Boston, Massachusetts 02111, USA
    Nat Rev Microbiol 6:913-24. 2008
    ..Here, we discuss the intertwined histories of EBV and BL and their relationship to the cofactors in BL pathogenesis: malaria and the MYC translocation...
  28. pmc A multifactorial role for P. falciparum malaria in endemic Burkitt's lymphoma pathogenesis
    Charles Torgbor
    Tufts University School of Medicine, Boston, Massachusetts, United States of America Department of Biochemistry and Biotechnology, Kwame Nkrumah University of Science and Technology KNUST and Kumasi Centre for Collaborative Research, Kumasi, Ghana
    PLoS Pathog 10:e1004170. 2014
    ..We propose that these activities combine synergistically to dramatically increase the incidence of eBL in individuals infected with malaria. ..
  29. pmc EBV microRNA BART 18-5p targets MAP3K2 to facilitate persistence in vivo by inhibiting viral replication in B cells
    Jin Qiu
    Department of Pathology, Tufts University School of Medicine, Boston, MA 02111
    Proc Natl Acad Sci U S A 111:11157-62. 2014
    ..We propose that the role of 18-5p is to maintain latency by reducing the risk of fortuitous reactivation of the virus in latently infected memory B cells. ..
  30. pmc A virtual look at Epstein-Barr virus infection: biological interpretations
    Karen A Duca
    Virginia Bioinformatics Institute, Virginia Polytechnic and State University, Blacksburg, Virginia, USA
    PLoS Pathog 3:1388-400. 2007
    ....
  31. ncbi request reprint Pathogens cooperate in lymphomagenesis
    David A Thorley-Lawson
    Nat Med 13:906-7. 2007

Research Grants48

  1. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2001
    ..Are virus infected cells in the lymphoid tissue able to undergo a germinal center reaction to enter the memory compartment. ..
  2. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2002
    ..4. Use mouse model systems to study how LMP2 positive cells may escape immunosurveillance (LMP2 transgenics), and identify the potentially oncogenic populations in immunosuppressed donors (SCID mice). ..
  3. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 1999
    ..4. Use mouse model systems to study how LMP2 positive cells may escape immunosurveillance (LMP2 transgenics), and identify the potentially oncogenic populations in immunosuppressed donors (SCID mice). ..
  4. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2003
    ..However, epithelial tissues are biologically diverse so we will focus our studies on the biologically relevant epithelium from the tonsil. ..
  5. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2003
    ..Are virus infected cells in the lymphoid tissue able to undergo a germinal center reaction to enter the memory compartment. ..
  6. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2000
    ..Are virus infected cells in the lymphoid tissue able to undergo a germinal center reaction to enter the memory compartment. ..
  7. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2006
    ..Specifically this approach will be used to identify genes and signaling pathways activated by LMP1. This will provide a molecular basis for explaining the role of LMP1 in NPC. ..
  8. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2006
    ..However, epithelial tissues are biologically diverse so we will focus our studies on the biologically relevant epithelium from the tonsil. ..
  9. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2002
    ..Are virus infected cells in the lymphoid tissue able to undergo a germinal center reaction to enter the memory compartment. ..
  10. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2004
    ..Specifically this approach will be used to identify genes and signaling pathways activated by LMP1. This will provide a molecular basis for explaining the role of LMP1 in NPC. ..
  11. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2005
    ..Specifically this approach will be used to identify genes and signaling pathways activated by LMP1. This will provide a molecular basis for explaining the role of LMP1 in NPC. ..
  12. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 2007
    ..Specifically this approach will be used to identify genes and signaling pathways activated by LMP1. This will provide a molecular basis for explaining the role of LMP1 in NPC. ..
  13. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2004
    ..However, epithelial tissues are biologically diverse so we will focus our studies on the biologically relevant epithelium from the tonsil. ..
  14. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2005
    ..However, epithelial tissues are biologically diverse so we will focus our studies on the biologically relevant epithelium from the tonsil. ..
  15. Computer Simulation of Epstein Barr Virus Infection
    David Thorley Lawson; Fiscal Year: 2006
    ..e. cure) of the virus is realistic or even possible. ..
  16. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2001
    ..4. Use mouse model systems to study how LMP2 positive cells may escape immunosurveillance (LMP2 transgenics), and identify the potentially oncogenic populations in immunosuppressed donors (SCID mice). ..
  17. Computer Simulation of Epstein Barr Virus Infection
    David Thorley Lawson; Fiscal Year: 2007
    ..e. cure) of the virus is realistic or even possible. ..
  18. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2007
    ..However, epithelial tissues are biologically diverse so we will focus our studies on the biologically relevant epithelium from the tonsil. ..
  19. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 1992
    ..Lastly, tumor cell lines will be tested for the presence of integrated EBV genomes by the fluorescence in situ hybridization technique to provide a definitive answer as to whether such sequences are or are not present...
  20. EPSTEIN BARR VIRUS LATENCY
    David A Thorley Lawson; Fiscal Year: 2010
    ..abstract_text> ..
  21. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David A Thorley Lawson; Fiscal Year: 2010
    ..These will be tested for autoreactivity by ELISA and immunofluorescence techniques on standard sources of autoantigens. This will answer the question of whether or not EBV promotes the survival of autoreactive B cells in vivo. ..
  22. EPSTEIN BARR VIRUS LATENCY
    David Thorley Lawson; Fiscal Year: 1999
    ..Are virus infected cells in the lymphoid tissue able to undergo a germinal center reaction to enter the memory compartment. ..
  23. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 1993
    ..Lastly, tumor cell lines will be tested for the presence of integrated EBV genomes by the fluorescence in situ hybridization technique to provide a definitive answer as to whether such sequences are or are not present...
  24. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2009
    ..These will be tested for autoreactivity by ELISA and immunofluorescence techniques on standard sources of autoantigens. This will answer the question of whether or not EBV promotes the survival of autoreactive B cells in vivo. ..
  25. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 1990
    ..These studies should help us understand at the molecular level, mechanisms involved when EBV infects and activated B cells and how the healthy immune response eliminates the infected cells...
  26. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 1991
    ..Lastly, tumor cell lines will be tested for the presence of integrated EBV genomes by the fluorescence in situ hybridization technique to provide a definitive answer as to whether such sequences are or are not present...
  27. Computer Simulation of Epstein Barr Virus Infection
    David Thorley Lawson; Fiscal Year: 2009
    ..e. cure) of the virus is realistic or even possible. ..
  28. LSRII Four Laser Analytical Flow Cytometer
    David Thorley Lawson; Fiscal Year: 2006
    ..This renders the acquisition of a new LSR II essential, if we are to meet the flow cytometry needs, both in time and available technology, for the community of NIH funded researchers at TUSM and T-NEMC. ..
  29. HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO
    David Thorley Lawson; Fiscal Year: 2000
    ..4. Use mouse model systems to study how LMP2 positive cells may escape immunosurveillance (LMP2 transgenics), and identify the potentially oncogenic populations in immunosuppressed donors (SCID mice). ..