# HOST CELL INTERACTION OF ANIMAL VIRUSES

> **NIH NIH R01** · UNIVERSITY OF CONNECTICUT STORRS · 1988 · $170,304

## Abstract

When humans, animals, birds or fish are infected by viruses, interferon is
induced.  The interferon system represents the most potent biological
mechanism for the control of virus replication, and the only one to prevent
cell-killing by otherwise lethal viruses.

The induction and production of interferon is exquisitely regulated.  A
single virus particle may induce the interferon genes to full production.
Another kind of virus particle may suppress interferon induction.  In the
longterm this research is designed to understand how viral double-stranded
RNA functions as the proximal inducer of interferon, what regulates the
induction/production process, and how, in turn, the interferon system acts
to prevent the lethal action of a virus and regulate host cell survival and
virus replication during persistent infection.

Specific aims include:  (1) The study of interferon induction by viruses,
by (i) establishing, in situ, double-stranded RNA as the proximal
interferon inducer, (ii) studying the regulation of interferon yield by
different viruses, (iii) defining the interferon inducer molecule for
adenovirus, and (iv) developing a model for defining interferon induction
dose.  (2) To study the mode of action of virus particles that suppress
interferon induction, (3) To test an hypothesis that silent mutations are
responsible for converting viruses from non-inducers to inducers of
interferon, (4) To study the involvement of prostaglandins and leukotrienes
in the development of interferon inducibility, (5) To characterize a novel
acid-labile chicken interferon, (6) To study a double-stranded RNA
inducible double-stranded ribonuclease discovered in aged chick embryo
cells, (7) To genetically clone 3'-transcribing defective-interfering
particles of vesicular stomatitis virus using a single-cell procedure, (8)
To develop an "absolute" test for genetic complementation between
temperature-sensitive viral mutants, (9) To determine how viruses kill
cells, and (10) To test further the role of the interferon system in
persistent infection.

To accomplish these goals we will continue to exploit a cell system that is
hyperresponsive to the induction process (aged primary chick embryo cells),
and a viral inducer for which one molecule of double-stranded RNA
represents the threshold for interferon induction (the [+-]RNA DI-011
particle of vesicular stomatitis virus).

## Key facts

- **NIH application ID:** 3127879
- **Project number:** 5R01AI018381-18
- **Recipient organization:** UNIVERSITY OF CONNECTICUT STORRS
- **SAM.gov UEI:** WNTPS995QBM7
- **Principal Investigator:** PHILIP Irving MARCUS
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $170,304
- **Award type:** 5
- **Project period:** 1981-07-01 → 1991-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3127879

## Citation

> US National Institutes of Health, RePORTER application 3127879, HOST CELL INTERACTION OF ANIMAL VIRUSES (5R01AI018381-18). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3127879. Licensed CC0.

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