Patricia M Day

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Identification of a role for the trans-Golgi network in human papillomavirus 16 pseudovirus infection
    Patricia M Day
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
    J Virol 87:3862-70. 2013
  2. pmc A human papillomavirus (HPV) in vitro neutralization assay that recapitulates the in vitro process of infection provides a sensitive measure of HPV L2 infection-inhibiting antibodies
    Patricia M Day
    Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Clin Vaccine Immunol 19:1075-82. 2012
  3. pmc Heparan sulfate-independent cell binding and infection with furin-precleaved papillomavirus capsids
    Patricia M Day
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    J Virol 82:12565-8. 2008
  4. pmc Establishment of papillomavirus infection is enhanced by promyelocytic leukemia protein (PML) expression
    Patricia M Day
    Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 101:14252-7. 2004
  5. pmc The role of furin in papillomavirus infection
    Patricia M Day
    Laboratory of Cellular Oncology, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Future Microbiol 4:1255-62. 2009
  6. pmc Neutralization of human papillomavirus with monoclonal antibodies reveals different mechanisms of inhibition
    Patricia M Day
    Laboratory of Cellular Oncology, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, USA
    J Virol 81:8784-92. 2007
  7. pmc Mechanisms of human papillomavirus type 16 neutralization by l2 cross-neutralizing and l1 type-specific antibodies
    Patricia M Day
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Virol 82:4638-46. 2008
  8. pmc In vivo mechanisms of vaccine-induced protection against HPV infection
    Patricia M Day
    Laboratory of Cellular Oncology, National Cancer Institute National Institutes of Health, Bethesda, MD 20892, USA
    Cell Host Microbe 8:260-70. 2010
  9. pmc Characterization of Mus musculus papillomavirus 1 infection in situ reveals an unusual pattern of late gene expression and capsid protein localization
    Alessandra Handisurya
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
    J Virol 87:13214-25. 2013
  10. pmc The initial steps leading to papillomavirus infection occur on the basement membrane prior to cell surface binding
    Rhonda C Kines
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 106:20458-63. 2009

Collaborators

Detail Information

Publications21

  1. pmc Identification of a role for the trans-Golgi network in human papillomavirus 16 pseudovirus infection
    Patricia M Day
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
    J Virol 87:3862-70. 2013
    ..Additionally, Rab9a and Rab7b were determined to be mediators of this transit, as expression of dominant negative versions of these proteins, but not Rab7a, significantly inhibited HPV16 pseudovirus infection...
  2. pmc A human papillomavirus (HPV) in vitro neutralization assay that recapitulates the in vitro process of infection provides a sensitive measure of HPV L2 infection-inhibiting antibodies
    Patricia M Day
    Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Clin Vaccine Immunol 19:1075-82. 2012
    ..This "L2-based" in vitro neutralization assay should prove useful in critically evaluating the immunogenicity of L2 vaccine candidates in preclinical studies and future clinical trials...
  3. pmc Heparan sulfate-independent cell binding and infection with furin-precleaved papillomavirus capsids
    Patricia M Day
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    J Virol 82:12565-8. 2008
    ..We conclude that the primary function of HSPG binding is to enable cell surface furin cleavage of L2 and that binding to a distinct cell surface receptor(s) is a subsequent step of papillomavirus infection...
  4. pmc Establishment of papillomavirus infection is enhanced by promyelocytic leukemia protein (PML) expression
    Patricia M Day
    Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 101:14252-7. 2004
    ..The results identify a role for PML in the enhancement of viral infectivity in the early part of the life cycle. We propose a model in which L2 chaperones the viral genome to ND10 to efficiently initiate viral transcription...
  5. pmc The role of furin in papillomavirus infection
    Patricia M Day
    Laboratory of Cellular Oncology, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Future Microbiol 4:1255-62. 2009
    ..This work also has implications for further advances in papillomavirus vaccine development...
  6. pmc Neutralization of human papillomavirus with monoclonal antibodies reveals different mechanisms of inhibition
    Patricia M Day
    Laboratory of Cellular Oncology, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, USA
    J Virol 81:8784-92. 2007
    ..We conclude that neutralizing antibodies can inhibit HPV infection by multiple distinct mechanisms, and understanding these mechanisms can add insight to the HPV entry processes...
  7. pmc Mechanisms of human papillomavirus type 16 neutralization by l2 cross-neutralizing and l1 type-specific antibodies
    Patricia M Day
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Virol 82:4638-46. 2008
    ..These findings suggest a dynamic model of virion-cell surface interactions that has implications for both evolution of viral serotypes and the efficacy of current and future HPV vaccines...
  8. pmc In vivo mechanisms of vaccine-induced protection against HPV infection
    Patricia M Day
    Laboratory of Cellular Oncology, National Cancer Institute National Institutes of Health, Bethesda, MD 20892, USA
    Cell Host Microbe 8:260-70. 2010
    ..Regardless of the concentration, L2 vaccine-induced antibodies allow BM association but prevent association with the cell surface. Thus, we have revealed distinct mechanisms of vaccine-induced inhibition of virus infection in vivo...
  9. pmc Characterization of Mus musculus papillomavirus 1 infection in situ reveals an unusual pattern of late gene expression and capsid protein localization
    Alessandra Handisurya
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
    J Virol 87:13214-25. 2013
    ....
  10. pmc The initial steps leading to papillomavirus infection occur on the basement membrane prior to cell surface binding
    Rhonda C Kines
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 106:20458-63. 2009
    ....
  11. pmc Murine skin and vaginal mucosa are similarly susceptible to infection by pseudovirions of different papillomavirus classifications and species
    Alessandra Handisurya
    Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Virology 433:385-94. 2012
    ....
  12. pmc Intravaginal immunization with HPV vectors induces tissue-resident CD8+ T cell responses
    Nicolas Cuburu
    Laboratory of Cellular Oncology, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    J Clin Invest 122:4606-20. 2012
    ..Thus, HPV vectors are attractive gene-delivery platforms for inducing durable intraepithelial cervicovaginal CD8+ T cell responses by promoting local proliferation and retention of primed antigen-specific CD8+ T cells...
  13. pmc Human alpha-defensins block papillomavirus infection
    Christopher B Buck
    Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute NIH, Bethesda, MD 20892 4263, USA
    Proc Natl Acad Sci U S A 103:1516-21. 2006
    ....
  14. pmc Role of heparan sulfate in attachment to and infection of the murine female genital tract by human papillomavirus
    Katherine M Johnson
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Virol 83:2067-74. 2009
    ..We speculate that cutaneous HPVs, such as HPV5, and genital mucosal HPVs, such as HPV16 and -31, may have evolved to recognize different forms of HSPGs to enable them to preferentially infect keratinocytes at different anatomical sites...
  15. pmc Cleavage of the papillomavirus minor capsid protein, L2, at a furin consensus site is necessary for infection
    Rebecca M Richards
    Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 103:1522-7. 2006
    ..However, to our knowledge, furin has not been previously implicated in the viral entry process. This step is potentially a target for PV inhibition...
  16. ncbi request reprint Papillomaviruses infect cells via a clathrin-dependent pathway
    Patricia M Day
    Laboratory of Cellular Oncology, Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Building 36, Room 1D 32, Bethesda, MD 20892, USA
    Virology 307:1-11. 2003
    ..Surprisingly, the kinetics of internalization were unusually slow for this mechanism, with the t(1/2) of entry of BPV-1 being approximately 4 h versus 5-15 min for a typical ligand...
  17. ncbi request reprint Interaction of papillomavirus virus-like particles with human myeloid antigen-presenting cells
    Petra Lenz
    Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 4040, USA
    Clin Immunol 106:231-7. 2003
    ..Our results indicate that VLPs target multiple cells of the immune system, which helps to account for VLPs being so effective in priming humoral and cellular immune responses even in the absence of adjuvant...
  18. pmc Current understanding of the mechanism of HPV infection
    John T Schiller
    Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892, USA
    Gynecol Oncol 118:S12-7. 2010
    ....
  19. pmc Cell surface-binding motifs of L2 that facilitate papillomavirus infection
    Rongcun Yang
    Department of Pathology, The Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA
    J Virol 77:3531-41. 2003
    ..Upon the binding of papillomavirus to the cell surface, residues 13 to 31 of L2 interact with a widely expressed, trypsin- and heparinase-resistant cell surface molecule and facilitate infection...
  20. pmc A membrane-destabilizing peptide in capsid protein L2 is required for egress of papillomavirus genomes from endosomes
    Nadine Kämper
    Institute of Medical Microbiology and Hygiene, Johannes Gutenberg Universitat Mainz, Germany
    J Virol 80:759-68. 2006
    ..Furthermore, the characteristic of this peptide differs from the classical virus-encoded membrane-penetrating peptides...
  21. pmc Human papillomavirus type 16 entry: retrograde cell surface transport along actin-rich protrusions
    Mario Schelhaas
    Institute of Biochemistry, ETH Zurich, Zurich, Switzerland
    PLoS Pathog 4:e1000148. 2008
    ..We found that transport along actin protrusions significantly enhanced HPV-16 infection in sparse tissue culture, cells suggesting a role for in vivo infection of basal keratinocytes during wound healing...