# CONTROL OF TRANSLATION IN POLIOVIRUS-INFECTED CELLS

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 1987 · $185,694

## Abstract

The aim of this research is to understand the mechanism by which poliovirus
infection causes a specific inhibition of host cell protein synthesis while
production of viral proteins proceeds efficiently.  Infected cell extracts
show a loss of the ability to translate capped mRNAs in vitro, although
they do function in the translation of viral RNA.  This is due to a
virus-induced inactivation of a specific translational initiation factor
(the cap binding protein complex) which recognizes and binds the 5' cap
group on cellular mRNAs, and seems to facilitate the binding of mRNA to the
40S ribosomal subunit.  Poliovirus mRNA is not capped and, therefore,
presumably can by-pass the requirement for the cap binding protein.
Studies proposed in this application will define the biochemical mechanism
of the inactivation of cap binding activity, and will result in the
purification and identification of the viral mediator of the inactivation
reaction.  Additional studies are proposed to define the mechanism of
ribosome binding and initiation of translation of poliovirus mRNA, which
occurs in the absence of a cap group.

## Key facts

- **NIH application ID:** 3125175
- **Project number:** 5R01AI012387-13
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **SAM.gov UEI:** LL8GLEVH6MG3
- **Principal Investigator:** Ellie R. Ehrenfeld
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $185,694
- **Award type:** 5
- **Project period:** 1975-05-01 → 1990-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3125175

## Citation

> US National Institutes of Health, RePORTER application 3125175, CONTROL OF TRANSLATION IN POLIOVIRUS-INFECTED CELLS (5R01AI012387-13). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3125175. Licensed CC0.

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