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Stephanie Jost

Researcher at Beth Israel Deaconess Medical Center

Publications -  47
Citations -  3261

Stephanie Jost is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Innate immune system & Immune system. The author has an hindex of 23, co-authored 42 publications receiving 2829 citations. Previous affiliations of Stephanie Jost include Massachusetts Institute of Technology & Ragon Institute of MGH, MIT and Harvard.

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Inhibition of hepatitis B virus replication by APOBEC3G

TL;DR: The human APOBEC3G is a cytidine deaminase that represents one such barrier, conferring broad intracellular antiretroviral protection as discussed by the authors, and is packaged in virions and, during reverse transcription, deaminates deoxycytidine.
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Control of Human Viral Infections by Natural Killer Cells

TL;DR: The role of NK cells in the control of four important viral infections in humans: cytomegalovirus, influenza virus, HIV-1, and hepatitis C virus is reviewed.
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A robust, high-throughput assay to determine the phagocytic activity of clinical antibody samples

TL;DR: In this paper, a robust and high-throughput flow cytometric assay was proposed to define the phagocytic activity of antigen-specific antibodies from clinical samples. But the authors did not consider the role of specific Fcγ-receptor subtypes.

A robust, high-throughput assay to determine the phagocytic activity of clinical antibody samples

TL;DR: A robust and high-throughput flow cytometric assay to define the phagocytic activity of antigen-specific antibodies from clinical samples, employing a monocytic cell line that expresses numerous Fc receptors: including inhibitory and activating, and high and low affinity receptors--allowing complex phenotypes to be studied.
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A Patient with HIV-1 Superinfection

TL;DR: An HIV-1–infected patient had a rebound in viremia when antiviral therapy was discontinued as part of a vaccine research protocol, and careful studies showed that this patient was infected initially with subtype AE of the virus but then became infected with sub type B.