Dr. Schnell Matthias J. Schnell, PhD

Contact Dr. Schnell

233 South 10th Street
531 BLSB
Philadelphia, PA 19107

(215) 503-4634
(215) 503-5393 fax

Research and Clinical Interests
Research interests of the laboratory are the development of novel vaccines and viral pathogenesis.

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Publications

Most recent Peer-reviewed Publications

  1. Rabies virus is recognized by the NLRP3 inflammasome and activates interleukin-1Β release in murine dendritic cells
  2. Interspecies protein substitution to investigate the role of the lyssavirus glycoprotein
  3. A replication-deficient rabies virus vaccine expressing Ebola virus glycoprotein is highly attenuated for neurovirulence
  4. Immune Clearance of Attenuated Rabies Virus Results in Neuronal Survival with Altered Gene Expression
  5. Further characterization of the immune response in mice to inactivated and live rabies vaccines expressing Ebola virus glycoprotein
  6. Targeted single-neuron infection with rabies virus for transneuronal multisynaptic tracing
  7. The role of micronutrients in the diet of HIV-1-infected individuals
  8. A role for granulocyte-macrophage colony-stimulating factor in the regulation of CD8+ T cell responses to rabies virus
  9. Proliferating cell nuclear antigen is required for loading of the SMCX/KMD5C histone demethylase onto chromatin
  10. Inactivated or live-attenuated bivalent vaccines that confer protection against rabies and Ebola viruses
  11. MicroRNA-122: a therapeutic target for hepatitis C virus (HCV) infection.
  12. Immunization of mice with the non-toxic HC50 domain of botulinum neurotoxin presented by rabies virus particles induces a strong immune response affording protection against high-dose botulinum neurotoxin challenge
  13. Rabies Virus as a Research Tool and Viral Vaccine Vector
  14. Rabies virus (RV) glycoprotein expression levels are not critical for pathogenicity of RV
  15. Dendritic cells infected by recombinant rabies virus vaccine vector expressing HIV-1 Gag are immunogenic even in the presence of vector-specific immunity
  16. Rabies virus infection induces type I interferon production in an IPS-1 dependent manner while dendritic cell activation relies on IFNAR signaling.
  17. Induction of neutralizing antibody responses to anthrax protective antigen by using influenza virus vectors: Implications for disparate immune system priming pathways
  18. Rabies virus infection induces type I interferon production in an IPS-1 dependent manner while dendritic cell activation relies on IFNAR signaling
  19. Characterization of a single-cycle rabies virus-based vaccine vector
  20. A novel composite immunotoxin that suppresses rabies virus production by the infected cells

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