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Raphaël M. Zellweger

Researcher at University of Oxford

Publications -  29
Citations -  1973

Raphaël M. Zellweger is an academic researcher from University of Oxford. The author has contributed to research in topics: Antibody & Dengue virus. The author has an hindex of 19, co-authored 23 publications receiving 1739 citations. Previous affiliations of Raphaël M. Zellweger include University of Zurich & International Vaccine Institute.

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A Protective Role for Dengue Virus-Specific CD8+ T Cells

TL;DR: An important role for CD8+ T cells in the host defense against DENV is revealed and it is demonstrated that the anti-DENV CD8- T cell response can be enhanced by immunization, providing rationale for designing DENV-specific vaccines that induce cell-mediated immunity.
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Enhanced Infection of Liver Sinusoidal Endothelial Cells in a Mouse Model of Antibody-Induced Severe Dengue Disease

TL;DR: It is demonstrated in mice that DENV-specific antibodies can sufficiently increase severity of disease so that a mostly nonlethal illness becomes a fatal disease resembling human DHF/DSS.
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CD4 + T Cells Are Not Required for the Induction of Dengue Virus-Specific CD8 + T Cell or Antibody Responses but Contribute to Protection after Vaccination

TL;DR: It is concluded that whereas CD4+ T cells are not required for controlling primary DENV infection, their induction by immunization can contribute to viral clearance and suggest inducing anti-DENV CD4- T cell responses by vaccination may be beneficial.
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A current perspective on antimicrobial resistance in Southeast Asia.

TL;DR: The current AMR situation in Southeast Asia is described, the mechanisms that make Southeast Asia a focal region for the emergence of AMR are explored, and ways in which Southeast Asia could contribute to a global solution are proposed.
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A Mouse-Passaged Dengue Virus Strain with Reduced Affinity for Heparan Sulfate Causes Severe Disease in Mice by Establishing Increased Systemic Viral Loads

TL;DR: A recombinant virus is described, differing from the non-mouse-passaged virus by two mutations in the E protein, that induces vascular leakage and tumor necrosis factor alpha (TNF-α)-mediated lethality, while the other virus causes paralysis.