# Functions of translation regulation in host susceptibility to virus infection

> **NIH NIH F32** · ROCKEFELLER UNIVERSITY · 2020 · $69,306

## Abstract

PROJECT SUMMARY/ABSTRACT
 Translation is a critical stage at which the abundance, timing, and localization of gene expression is
regulated. In the case of infection, precise control of translational machinery and processes can determine
whether an effective antiviral program is initiated or whether these programs are impeded by the invading
pathogen. Although required for both virus replication and host defense, mechanisms by which translation is
regulated early after virus infection are not fully understood. Moreover, the importance of translational
regulation in limiting viral replication remains to be elucidated. Understanding functions for translational
regulation during virus infection and innate immune responses will provide insights into virus-induced disease
and uncover novel mechanisms of antiviral immunity. The main goal of this proposal is to investigate
functions of early regulation of translation in host susceptibility to virus infection. In Specific Aim 1, I
will use ribosome profiling and pulse-labeled mass spectrometry to identify and quantify translationally
regulated mRNAs in immune stimulated cells. Cells deficient for specific translationally regulated mRNAs will
be used to determine the importance of these mRNAs in viral replication and antiviral immunity. In Specific
Aim 2, I will utilize confocal microscopy of pulse-labeled cells to define subcellular sites of early translational
events that follow virus infection and immune activation. Translation of specific antiviral mRNAs also will be
examined by selective tagging and visualized by live-cell microscopy. In Specific Aim 3, I will study ribosomal
stalk proteins, which were recently identified as pro-viral host factors in a CRISPR knockout screen, and their
roles during virus infection. Expression and localization of the stalk proteins will be determined following
immune stimulation, and translation and viral replication will be assessed in stalk protein-deficient cells. Stalk
protein-deficient cells will be reconstituted with genetically altered constructs to define sequences that
contribute to stalk protein function. Together, these studies will elucidate functions for translational regulation in
host susceptibility to virus infection and will enhance our understanding of host-pathogen interactions.
Knowledge gained from this proposed research may illuminate new approaches for therapeutically targeting
broad families of viruses.

## Key facts

- **NIH application ID:** 9868280
- **Project number:** 5F32AI133910-03
- **Recipient organization:** ROCKEFELLER UNIVERSITY
- **Principal Investigator:** Alison Whitney Ashbrook
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $69,306
- **Award type:** 5
- **Project period:** 2018-03-01 → 2021-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9868280

## Citation

> US National Institutes of Health, RePORTER application 9868280, Functions of translation regulation in host susceptibility to virus infection (5F32AI133910-03). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9868280. Licensed CC0.

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