# GENE REGULATION OF MAMMALIAN DNA VIRUSES

> **NIH NIH R01** · UNIVERSITY OF FLORIDA · 1989 · $240,842

## Abstract

We will focus on three areas of poxvirus molecular biology:  (1)
the mechanism by which these viruses selectively mobilize
nuclear components to the cytoplasm and whether proteins to be
mobilized are modified; (2) the enzymology of late viral gene
transcription and the role in this process of host cell RNA
polymerase II (Pol II); and (3) the identification and elimination of
viral genes associated with various pathogenic properties of the
virus.  The sensitivity of poxvirus infections to alpha-amanitin and
the failure of the virus to grow in enucleated cells suggest that
cellular Pol II is required for virus production.  We have shown
that poxviruses induce translocation of the largest subunit of Pol
II to the cytoplasm.  A study of the mechanism by which poxvirus
recruits nuclear components necessitates an assay for the ability
of viral components to induce translocation.  We hope to achieve
this by:  (1) microinjection into frog oocytes or mammalian cells;
(2) fusion with yeast spheroplasts; or (3) the addition of viral
components directly to isolated nuclei.  To investigate the
enzymology and the role of Pol II in late viral gene transcription,
we will continue to prepare or obtain monoclonal antibodies to Pol
II and the viral RNA polymerase.  The antibodies, coupled with
enzyme assays will allow us to follow the fates of viral and host
RNA polymerase subunits during the later phases of infection to
gain insight about the composition and function of the late
transcription complex.  Ultimately, we wish to purify a complex
capable of late promoter recognition in vitro.  Another major goal
is to study the molecular basis of pathogenesis of poxviruses.
Identification of genes associated with aspects of poxvirus
pathogenesis is timely because of the interest in recombinant
vaccinia viruses as vaccine vectors.  We describe an avirulent
virus deletion mutant which grows only locally during
scarification and is incapable of growth within the CNS or viscera
of animals.  We will engineer this mutant to contain a unique site
for reinsertion of the deleted regions and thereby identify the
genes which permit the virus to grow within the CNS and viscera.
We will try to correlate increases in pathogenesis with changes in
host range in culture which might serve as a simple index of
potential vaccine complications and side effects.

## Key facts

- **NIH application ID:** 3126385
- **Project number:** 5R01AI015722-11
- **Recipient organization:** UNIVERSITY OF FLORIDA
- **SAM.gov UEI:** NNFQH1JAPEP3
- **Principal Investigator:** Richard W Moyer
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $240,842
- **Award type:** 5
- **Project period:** 1987-02-01 → 1993-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3126385

## Citation

> US National Institutes of Health, RePORTER application 3126385, GENE REGULATION OF MAMMALIAN DNA VIRUSES (5R01AI015722-11). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3126385. Licensed CC0.

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