CHRISTOPHER BASLER

Summary

Affiliation: Mount Sinai School of Medicine
Country: USA

Publications

  1. pmc Marburg virus evades interferon responses by a mechanism distinct from ebola virus
    Charalampos Valmas
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York, USA
    PLoS Pathog 6:e1000721. 2010
  2. pmc An upstream open reading frame modulates ebola virus polymerase translation and virus replication
    Reed S Shabman
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York, United States of America
    PLoS Pathog 9:e1003147. 2013
  3. pmc Phylogenetics and pathogenesis of early avian influenza viruses (H5N1), Nigeria
    Comfort O Aiki-Raji
    University of Ibadan, Ibadan, Nigeria
    Emerg Infect Dis 14:1753-5. 2008
  4. doi request reprint A novel mechanism of immune evasion mediated by Ebola virus soluble glycoprotein
    Christopher F Basler
    Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
    Expert Rev Anti Infect Ther 11:475-8. 2013
  5. ncbi request reprint Nipah and hendra virus interactions with the innate immune system
    Christopher F Basler
    Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029, USA
    Curr Top Microbiol Immunol 359:123-52. 2012
  6. pmc Progress in identifying virulence determinants of the 1918 H1N1 and the Southeast Asian H5N1 influenza A viruses
    Christopher F Basler
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, United States
    Antiviral Res 79:166-78. 2008
  7. ncbi request reprint Influenza viruses: basic biology and potential drug targets
    Christopher F Basler
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    Infect Disord Drug Targets 7:282-93. 2007
  8. pmc The Ebola virus VP35 protein inhibits activation of interferon regulatory factor 3
    Christopher F Basler
    Department of Microbiology, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    J Virol 77:7945-56. 2003
  9. pmc Evasion of interferon responses by Ebola and Marburg viruses
    Christopher F Basler
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Interferon Cytokine Res 29:511-20. 2009
  10. pmc A novel paramyxovirus?
    Christopher F Basler
    Department of Microbiology, Mount Sinai School of Medicine, Box 1124, New York, NY 10029, USA
    Emerg Infect Dis 11:108-12. 2005

Research Grants

  1. EBOLA VIRUS INTERFERON-ANTAGONISTS AND VIRULENCE
    CHRISTOPHER BASLER; Fiscal Year: 2003
  2. Lassa and Nipah Virus Interferon-Antagonists
    CHRISTOPHER BASLER; Fiscal Year: 2003
  3. Ebola VP35 Interferon-Antagonist: Mechanism and Signif
    CHRISTOPHER BASLER; Fiscal Year: 2009
  4. Ebola virus VP24_a novel inhibitor of interferon and oxidative stress signaling
    Christopher F Basler; Fiscal Year: 2011
  5. Ebola VP35 Interferon-Antagonist: Mechanism and Signif
    CHRISTOPHER BASLER; Fiscal Year: 2005
  6. Ebola VP35 Interferon-Antagonist: Mechanism and Signif
    CHRISTOPHER BASLER; Fiscal Year: 2006
  7. Ebola VP35 Interferon-Antagonist: Mechanism and Signif
    CHRISTOPHER BASLER; Fiscal Year: 2007
  8. Ebola VP35 Interferon-Antagonist: Mechanism and Signif
    CHRISTOPHER BASLER; Fiscal Year: 2009

Collaborators

Detail Information

Publications51

  1. pmc Marburg virus evades interferon responses by a mechanism distinct from ebola virus
    Charalampos Valmas
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York, USA
    PLoS Pathog 6:e1000721. 2010
    ..It identifies a novel function for the MARV VP40 protein and suggests that MARV may globally inhibit Jak1-dependent cytokine signaling...
  2. pmc An upstream open reading frame modulates ebola virus polymerase translation and virus replication
    Reed S Shabman
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York, United States of America
    PLoS Pathog 9:e1003147. 2013
    ..Cumulatively, these data identify novel mechanisms by which EBOV regulates its polymerase expression, demonstrate their relevance to virus replication and identify a potential therapeutic target...
  3. pmc Phylogenetics and pathogenesis of early avian influenza viruses (H5N1), Nigeria
    Comfort O Aiki-Raji
    University of Ibadan, Ibadan, Nigeria
    Emerg Infect Dis 14:1753-5. 2008
    ..Sequencing and phylogenetic analysis placed them within H5N1 subclade 2.2.2. Intravenous and intranasal pathogenicity tests produced systemic disease with vascular endothelial cell tropism in chickens...
  4. doi request reprint A novel mechanism of immune evasion mediated by Ebola virus soluble glycoprotein
    Christopher F Basler
    Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
    Expert Rev Anti Infect Ther 11:475-8. 2013
    ..Therefore, the production of sGP may prevent effective neutralization of the virus during Ebola virus infection, and may reduce the effectiveness of vaccines that rely upon neutralizing antibody responses...
  5. ncbi request reprint Nipah and hendra virus interactions with the innate immune system
    Christopher F Basler
    Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029, USA
    Curr Top Microbiol Immunol 359:123-52. 2012
    ..With these systems in hand, the field is now poised to define how specific viral IFN-antagonist functions influence viral pathogenesis...
  6. pmc Progress in identifying virulence determinants of the 1918 H1N1 and the Southeast Asian H5N1 influenza A viruses
    Christopher F Basler
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, United States
    Antiviral Res 79:166-78. 2008
    ..Defining how individual viral proteins promote enhanced replication, inflammation and severe disease will provide insight into the pathogenesis of severe influenza virus infections and suggest novel therapeutic approaches...
  7. ncbi request reprint Influenza viruses: basic biology and potential drug targets
    Christopher F Basler
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    Infect Disord Drug Targets 7:282-93. 2007
    ..However, the replication cycle of influenza viruses has been intensively studied and is receiving increased attention. New opportunities exist to develop novel antiviral strategies targeting these viruses...
  8. pmc The Ebola virus VP35 protein inhibits activation of interferon regulatory factor 3
    Christopher F Basler
    Department of Microbiology, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    J Virol 77:7945-56. 2003
    ..These data suggest that in Ebola virus-infected cells, VP35 inhibits the induction of antiviral genes, including the IFN-beta gene, by blocking IRF-3 activation...
  9. pmc Evasion of interferon responses by Ebola and Marburg viruses
    Christopher F Basler
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Interferon Cytokine Res 29:511-20. 2009
    ..Thus, despite their similarities, there are fundamental differences by which these deadly viruses counteract the IFN system. It will be of interest to determine how these differences influence pathogenesis...
  10. pmc A novel paramyxovirus?
    Christopher F Basler
    Department of Microbiology, Mount Sinai School of Medicine, Box 1124, New York, NY 10029, USA
    Emerg Infect Dis 11:108-12. 2005
    ..These genes are sufficiently unique to suggest the existence of a novel paramyxovirus genus...
  11. pmc Nipah virus V and W proteins have a common STAT1-binding domain yet inhibit STAT1 activation from the cytoplasmic and nuclear compartments, respectively
    Megan L Shaw
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, One Gustave L Levy Pl, New York, NY 10029, USA
    J Virol 78:5633-41. 2004
    ..We also show that the IFN antagonist activity of the P protein is not as strong as that of V or W, perhaps explaining why Nipah virus has evolved to express these two edited products...
  12. pmc Mutations abrogating VP35 interaction with double-stranded RNA render Ebola virus avirulent in guinea pigs
    Kathleen C Prins
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Virol 84:3004-15. 2010
    ..Moreover, these studies provide a framework for the development of antivirals targeting this critical EBOV virulence factor...
  13. pmc The tumour suppressor CYLD is a negative regulator of RIG-I-mediated antiviral response
    Constantin S Friedman
    Immunology Institute, Mount Sinai School of Medicine, Box 1630, One Gustave L Levy Place, New York, New York 10029, USA
    EMBO Rep 9:930-6. 2008
    ..These findings show that CYLD is a negative regulator of RIG-I-mediated innate antiviral response...
  14. pmc Newcastle disease virus V protein is a determinant of host range restriction
    Man Seong Park
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Virol 77:9522-32. 2003
    ..Taken together, these data suggest that the host range of NDV is limited by the ability of its V protein to efficiently prevent innate host defenses, such as the IFN response and apoptosis...
  15. pmc Ebola virus VP35 protein binds double-stranded RNA and inhibits alpha/beta interferon production induced by RIG-I signaling
    Washington B Cardenas
    Department of Microbiology, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    J Virol 80:5168-78. 2006
    ..These data support the hypothesis that dsRNA binding may contribute to VP35 IFN antagonist function. However, additional mechanisms of inhibition, at a point proximal to the IRF-3 kinases, most likely also exist...
  16. pmc A five-amino-acid deletion of the eastern equine encephalitis virus capsid protein attenuates replication in mammalian systems but not in mosquito cells
    Patricia V Aguilar
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    J Virol 82:6972-83. 2008
    ..This region is also critical for EEEV pathogenesis...
  17. ncbi request reprint Homo-oligomerization facilitates the interferon-antagonist activity of the ebolavirus VP35 protein
    St Patrick Reid
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    Virology 341:179-89. 2005
    ....
  18. pmc Nuclear localization of the Nipah virus W protein allows for inhibition of both virus- and toll-like receptor 3-triggered signaling pathways
    Megan L Shaw
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, One Gustave L Levy Pl, New York, NY 10029, USA
    J Virol 79:6078-88. 2005
    ....
  19. pmc Effects of influenza A virus NS1 protein on protein expression: the NS1 protein enhances translation and is not required for shutoff of host protein synthesis
    Mirella Salvatore
    Department of Microbiology Immunobiology Center, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Virol 76:1206-12. 2002
    ..In contrast to the earlier proposal suggesting that the NS1 protein regulates the levels of spliced M2 mRNA, no effects on M2 protein accumulation were seen in Vero cells infected with delNS1 virus...
  20. ncbi request reprint Neutralizing anti-influenza virus monoclonal antibodies: therapeutics and tools for discovery
    Osvaldo Martinez
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York, USA
    Int Rev Immunol 28:69-92. 2009
    ....
  21. pmc A recombinant influenza A virus expressing an RNA-binding-defective NS1 protein induces high levels of beta interferon and is attenuated in mice
    Nicola R Donelan
    Department of Microbiology Microbiology Graduate School Training Program, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Virol 77:13257-66. 2003
    ..These results suggest not only that the IFN antagonist properties of the NS1 protein depend on its ability to bind dsRNA but also that they can be modulated by amino acid residues not involved in RNA binding...
  22. pmc Nipah virus sequesters inactive STAT1 in the nucleus via a P gene-encoded mechanism
    Michael J Ciancanelli
    Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029, USA
    J Virol 83:7828-41. 2009
    ..These data demonstrate that the gene for NiV P encodes functions that sequester inactive STAT1 in the nucleus, preventing its activation and suggest that the W protein is the dominant inhibitor of STAT1 in NiV-infected cells...
  23. pmc Ebola virus protein VP35 impairs the function of interferon regulatory factor-activating kinases IKKepsilon and TBK-1
    Kathleen C Prins
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Virol 83:3069-77. 2009
    ....
  24. pmc Hemagglutinin-pseudotyped green fluorescent protein-expressing influenza viruses for the detection of influenza virus neutralizing antibodies
    Luis Martinez-Sobrido
    Department of Microbiology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    J Virol 84:2157-63. 2010
    ..These GFP-expressing influenza viruses replicate to high titers in HA-expressing cell lines, but in non-HA-expressing cells, their replication is restricted to a single cycle...
  25. pmc Capsid protein of eastern equine encephalitis virus inhibits host cell gene expression
    Patricia V Aguilar
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    J Virol 81:3866-76. 2007
    ....
  26. pmc Newcastle disease virus (NDV)-based assay demonstrates interferon-antagonist activity for the NDV V protein and the Nipah virus V, W, and C proteins
    Man Seong Park
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Virol 77:1501-11. 2003
    ....
  27. pmc The N- and C-terminal domains of the NS1 protein of influenza B virus can independently inhibit IRF-3 and beta interferon promoter activation
    Nicola R Donelan
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Pl, New York, NY 10029, USA
    J Virol 78:11574-82. 2004
    ..Our results support the hypothesis that the NS1 protein of influenza B virus plays an important role in antagonizing the IRF-3- and IFN-induced antiviral host responses to virus infection...
  28. pmc Functional replacement of the carboxy-terminal two-thirds of the influenza A virus NS1 protein with short heterologous dimerization domains
    Xiuyan Wang
    Department of Microbiology, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    J Virol 76:12951-62. 2002
    ..These results suggest that the main biological function of the carboxy-terminal region of the NS1 protein of influenza A virus is the enhancement of its IFN antagonist properties by stabilizing the NS1 dimeric structure...
  29. pmc Ebola virus VP24 binds karyopherin alpha1 and blocks STAT1 nuclear accumulation
    St Patrick Reid
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    J Virol 80:5156-67. 2006
    ..These data suggest that VP24 is likely to be an important virulence determinant that allows EBOV to evade the antiviral effects of IFNs...
  30. pmc Nipah virus edits its P gene at high frequency to express the V and W proteins
    Sachin Kulkarni
    Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029, USA
    J Virol 83:3982-7. 2009
    ..Eighty-two percent of transcripts are edited, with up to 11 G insertions observed. This exceptionally high editing frequency ensures expression of the V and W proteins...
  31. pmc A single amino acid substitution in 1918 influenza virus hemagglutinin changes receptor binding specificity
    Laurel Glaser
    Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029, USA
    J Virol 79:11533-6. 2005
    ..Mutation of this single amino acid back to the avian consensus resulted in a preference for the avian receptor...
  32. pmc Protection of mice against lethal challenge with 2009 H1N1 influenza A virus by 1918-like and classical swine H1N1 based vaccines
    Balaji Manicassamy
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York, United States of America
    PLoS Pathog 6:e1000745. 2010
    ..Our results also support the notion that pigs can act as an animal reservoir where influenza virus HAs become antigenically frozen for long periods of time, facilitating the generation of human pandemic viruses...
  33. pmc Ebola virus VP24 proteins inhibit the interaction of NPI-1 subfamily karyopherin alpha proteins with activated STAT1
    St Patrick Reid
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    J Virol 81:13469-77. 2007
    ....
  34. pmc Ebola virus-like particle-induced activation of NF-kappaB and Erk signaling in human dendritic cells requires the glycoprotein mucin domain
    Osvaldo Martinez
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    Virology 364:342-54. 2007
    ..We conclude that the GP mucin domain is required for VLPs to stimulate human dendritic cells through NF-kappaB and MAPK signaling pathways...
  35. pmc Mutation of YMYL in the Nipah virus matrix protein abrogates budding and alters subcellular localization
    Michael J Ciancanelli
    Department of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    J Virol 80:12070-8. 2006
    ..When YMYL was fused to a late-domain mutant of the Ebola virus VP40 matrix protein, VP40 budding was restored. These results suggest that the YMYL sequence may act as a trafficking signal and a late domain for NiV M...
  36. pmc Global host immune response: pathogenesis and transcriptional profiling of type A influenza viruses expressing the hemagglutinin and neuraminidase genes from the 1918 pandemic virus
    John C Kash
    Department of Microbiology, School of Medicine, University of Washington, Seattle, Washington 98195 8070, USA
    J Virol 78:9499-511. 2004
    ..These studies document clear differences in gene expression profiles that were correlated with pulmonary disease pathology induced by virulent and attenuated influenza virus infections...
  37. pmc Genomic analysis of increased host immune and cell death responses induced by 1918 influenza virus
    John C Kash
    Department of Microbiology, University of Washington School of Medicine, Seattle, Washington 98195, USA
    Nature 443:578-81. 2006
    ..Moreover, understanding the contribution of host immune responses to virulent influenza virus infections is an important starting point for the identification of prognostic indicators and the development of novel antiviral therapies...
  38. pmc Cellular transcriptional profiling in influenza A virus-infected lung epithelial cells: the role of the nonstructural NS1 protein in the evasion of the host innate defense and its potential contribution to pandemic influenza
    Gary K Geiss
    Department of Microbiology, School of Medicine, University of Washington, Seattle, WA 98195, USA
    Proc Natl Acad Sci U S A 99:10736-41. 2002
    ....
  39. pmc Zaire Ebola virus entry into human dendritic cells is insensitive to cathepsin L inhibition
    Osvaldo Martinez
    Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029, USA
    Cell Microbiol 12:148-57. 2010
    ..Thus, cathepsin L plays a minimal, if any, role in EBOV infection in human DCs. The inflammatory cytokine TNFalpha modulates cathepsin B activity and affects EBOV entry into and infection of human DCs...
  40. pmc Marburg virus VP40 antagonizes interferon signaling in a species-specific manner
    Charalampos Valmas
    Department Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L Levy Place, New York, NY 10029, USA
    J Virol 85:4309-17. 2011
    ..These data identify an apparent determinant of RAVV host range and virulence and define specific genetic determinants of this function...
  41. pmc Chimeric influenza A viruses with a functional influenza B virus neuraminidase or hemagglutinin
    Astrid Flandorfer
    Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029, USA
    J Virol 77:9116-23. 2003
    ..Taken together, we show here that the absence of reassortment between influenza viruses belonging to different A and B types is not due to spike glycoprotein incompatibility at the level of the full-length NA or of the HA ectodomain...
  42. ncbi request reprint Viruses and the type I interferon antiviral system: induction and evasion
    Christopher F Basler
    Mount Sinai School of Medicine, Department of Microbiology, New York, NY, USA
    Int Rev Immunol 21:305-37. 2002
    ..Understanding the interplay between viral-encoded IFN antagonists and the interferon response will be essential if the therapeutic potential of IFNs is to be fully exploited...
  43. pmc Existing antivirals are effective against influenza viruses with genes from the 1918 pandemic virus
    Terrence M Tumpey
    Southeast Poultry Research Laboratory, United States Department of Agriculture, Athens, GA 30605, USA
    Proc Natl Acad Sci U S A 99:13849-54. 2002
    ..These data suggest that current antiviral strategies would be effective in curbing the dangers of a re-emergent 1918 or 1918-like virus...
  44. ncbi request reprint Structure of the uncleaved human H1 hemagglutinin from the extinct 1918 influenza virus
    James Stevens
    Department of Molecular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Science 303:1866-70. 2004
    ....
  45. ncbi request reprint The makings of a killer
    Peter Palese
    Nat Med 8:927-8. 2002
  46. ncbi request reprint Characterization of the reconstructed 1918 Spanish influenza pandemic virus
    Terrence M Tumpey
    Influenza Branch, Mailstop G 16, Division of Viral and Rickettsial Diseases DVRD, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, NE, Atlanta, GA 30333, USA
    Science 310:77-80. 2005
    ..Moreover, the coordinated expression of the 1918 virus genes most certainly confers the unique high-virulence phenotype observed with this pandemic virus...
  47. pmc Single gene reassortants identify a critical role for PB1, HA, and NA in the high virulence of the 1918 pandemic influenza virus
    Claudia Pappas
    Influenza Division, Mailstop G 16, National Center for Immunization and Respiratory Diseases, Coordinating Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road Northeast, Atlanta, GA 30333, USA
    Proc Natl Acad Sci U S A 105:3064-9. 2008
    ..These results highlight the importance of the 1918 HA, NA, and PB1 genes for optimal virus replication and virulence of this pandemic strain...
  48. pmc Pathogenicity and immunogenicity of influenza viruses with genes from the 1918 pandemic virus
    Terrence M Tumpey
    Southeast Poultry Research Laboratory, Agricultural Research Service, U S Department of Agriculture, Athens, GA 30605, USA
    Proc Natl Acad Sci U S A 101:3166-71. 2004
    ..These data suggest a strategy of vaccination that would be effective against a reemergent 1918 or 1918-like virus...
  49. pmc Neutralizing antibodies derived from the B cells of 1918 influenza pandemic survivors
    Xiaocong Yu
    Departments of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA
    Nature 455:532-6. 2008
    ....
  50. pmc Pathogenicity of influenza viruses with genes from the 1918 pandemic virus: functional roles of alveolar macrophages and neutrophils in limiting virus replication and mortality in mice
    Terrence M Tumpey
    Influenza Branch, Mail Stop G 16, DVRD, NCID, Centers for Disease Control and Prevention, 1600 Clifton Road, N E, Atlanta, GA 30333, USA
    J Virol 79:14933-44. 2005
    ....
  51. ncbi request reprint Sensing RNA virus infections
    Christopher F Basler
    Nat Chem Biol 3:20-1. 2007

Research Grants9

  1. EBOLA VIRUS INTERFERON-ANTAGONISTS AND VIRULENCE
    CHRISTOPHER BASLER; Fiscal Year: 2003
    ..VP35 and VP24 may also prove to be attractive targets for new antiviral agents. Inhibition of anti-IFN factors may sensitize Ebola virus infected cells to the antiviral effects of IFN and may also enhance the effect of antiviral agents. ..
  2. Lassa and Nipah Virus Interferon-Antagonists
    CHRISTOPHER BASLER; Fiscal Year: 2003
    ..abstract_text> ..
  3. Ebola VP35 Interferon-Antagonist: Mechanism and Signif
    CHRISTOPHER BASLER; Fiscal Year: 2009
    ..abstract_text> ..
  4. Ebola virus VP24_a novel inhibitor of interferon and oxidative stress signaling
    Christopher F Basler; Fiscal Year: 2011
    ..The experiments in this proposal will clarify the role of two viral proteins, VP24 and VP35, in EBOV disease and suggest new ways to prevent or treat these infections. ..
  5. Ebola VP35 Interferon-Antagonist: Mechanism and Signif
    CHRISTOPHER BASLER; Fiscal Year: 2005
    ..abstract_text> ..
  6. Ebola VP35 Interferon-Antagonist: Mechanism and Signif
    CHRISTOPHER BASLER; Fiscal Year: 2006
    ..abstract_text> ..
  7. Ebola VP35 Interferon-Antagonist: Mechanism and Signif
    CHRISTOPHER BASLER; Fiscal Year: 2007
    ..abstract_text> ..
  8. Ebola VP35 Interferon-Antagonist: Mechanism and Signif
    CHRISTOPHER BASLER; Fiscal Year: 2009
    ..abstract_text> ..