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Peter J. Bredenbeek

Researcher at Leiden University Medical Center

Publications -  39
Citations -  3721

Peter J. Bredenbeek is an academic researcher from Leiden University Medical Center. The author has contributed to research in topics: Virus & Flavivirus. The author has an hindex of 24, co-authored 36 publications receiving 3280 citations. Previous affiliations of Peter J. Bredenbeek include Leiden University & Rockefeller University.

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Unique and conserved features of genome and proteome of SARS-coronavirus, an early split-off from the coronavirus group 2 lineage.

TL;DR: These newly recognized viral enzymes place the mechanism of coronavirus RNA synthesis in a completely new perspective and will be important targets for the design of antiviral strategies aimed at controlling the further spread of SARS-CoV.
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A stable full-length yellow fever virus cDNA clone and the role of conserved RNA elements in flavivirus replication.

TL;DR: The successful construction of a full-length infectious cDNA clone of the vaccine strain YF-17D is reported, which will aid future studies on YF replication and pathogenesis, as well as facilitate the development of YF -17D-based recombinant vaccines.
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The Enzymatic Activity of the nsp14 Exoribonuclease Is Critical for Replication of MERS-CoV and SARS-CoV-2.

TL;DR: This study strongly suggests that CoV nsp14 ExoN has an additional function, which apparently is critical for primary viral RNA synthesis and thus differs from the proofreading function that, based on previous MHV and SARS-CoV studies, was proposed to boost longer-term replication fidelity.
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Almost the entire 5′ non-translated region of hepatitis C virus is required for cap-independent translation

TL;DR: It is demonstrated that HCV 5′UTR driven translation is stimulated by poliovirus 2Apro co‐expression, and each of the predicted hairpins is found to be essential for cap‐independent translation.
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Middle East Respiratory Coronavirus Accessory Protein 4a Inhibits PKR-Mediated Antiviral Stress Responses.

TL;DR: It is shown that cellular infection with MERS-CoV does not lead to the formation of SGs and that p4a suppressing the PKR-dependent stress response pathway, probably by sequestering dsRNA.