Jacob Yount

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Associate Professor

Ohio State University

United States

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About

Jacob Yount is an Associate Professor at The Ohio State University in the United States. His research focuses on immunology and virology, particularly in relation to SARS-CoV-2 and T cell programming. Recent articles highlight his work on viral infection mechanisms and the immune response, including studies on the regulation of CD4+ T cells and the development of vaccines to combat COVID-19 variants.

Recent Grants

Grant: Close

Inhibition of cell-to-cell fusion by interferon-induced proteins

Open Date: 2019-06-01

Close Date: 2021-05-31

Grant: Close

Mechanisms of Cardioprotection by the Innate Immune System During Influenza Virus Infections

Open Date: 2019-06-01

Close Date: 2021-05-31

Grant: Close

Mechanisms of innate resistance to virus infections

Open Date: 2017-02-01

Close Date: 2022-01-31

Grant: Close

Molecular Control of IFITM3 in Restricting Influenza Virus Infection

Open Date: 2015-03-01

Close Date: 2017-02-28

Grant: Close

Mechanistic analysis of a posttranslationally modified innate antiviral effector

Open Date: 2011-05-01

Close Date: 2016-04-30

Articles (20)

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2021

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2021

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2021

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2020

Collaborators (11)

Levent Sari

University of Texas Southwestern Medical School

UNITED STATES

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UNITED STATES

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Mona El Refaey

Ohio State University

UNITED STATES

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Maciej Pietrzak

Research Assistant Professor

Ohio State University

UNITED STATES

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Jacob Yount

Research Interests

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Recent Grants

Articles (20)

Cytotoxic Programming of CD4+ T Cells Is Regulated by Opposing Actions of the Related Transcription Factors Eos and Aiolos.

SAMHD1 impairs type I interferon induction through the MAVS, IKKε, and IRF7 signaling axis during viral infection.

The host anti-viral protein SAMHD1 suppresses NF-κB activation by interacting with the IKK complex during inflammatory responses and viral infection.

A next-generation intranasal trivalent MMS vaccine induces durable and broad protection against SARS-CoV-2 variants of concern.

Inhibiting the Deubiquitinase UCHL1 Reduces SARS-CoV-2 Viral Uptake by ACE2.

Prime-Pull Immunization of Mice with a BcfA-Adjuvanted Vaccine Elicits Sustained Mucosal Immunity That Prevents SARS-CoV-2 Infection and Pathology.

Aiolos represses CD4<sup>+</sup> T cell cytotoxic programming via reciprocal regulation of T<sub>FH</sub> transcription factors and IL-2 sensitivity.

Interferon-induced transmembrane protein 3 (IFITM3) limits lethality of SARS-CoV-2 in mice.

Influenza A virus modulates ACE2 expression and SARS-CoV-2 infectivity in human cardiomyocytes

BEX1 is a critical determinant of viral myocarditis.

Rapalogs downmodulate intrinsic immunity and promote cell entry of SARS-CoV-2.

Moderately pathogenic maternal influenza A virus infection disrupts placental integrity but spares the fetal brain

A bioorthogonal chemical reporter for fatty acid synthase-dependent protein acylation.

SERINC proteins potentiate antiviral type I IFN production and proinflammatory signaling pathways.

Inhibition of SARS-CoV-2 Infection by Human Defensin HNP1 and Retrocyclin RC-101.

A Methyltransferase-Defective Vesicular Stomatitis Virus-Based SARS-CoV-2 Vaccine Candidate Provides Complete Protection against SARS-CoV-2 Infection in Hamsters.

Viral transport media for COVID-19 testing.

Protein <i>S</i>-palmitoylation in immunity.

A safe and highly efficacious measles virus-based vaccine expressing SARS-CoV-2 stabilized prefusion spike.

Recombinant MG53 Protein Protects Mice from Lethal Influenza Virus Infection

Collaborators (11)

Levent Sari

Melissa Leonard

Patrick Collins

Li Wu

Hazem Ghoneim

Adrienne Antonson

Jesse Kwiek

Haichang Li

Milo M. Lin

Mona El Refaey

Maciej Pietrzak

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