# REGULATION OF HUMAN CYTOMEGALOVIRUS GENE EXPRESSION

> **NIH NIH R01** · UNIVERSITY OF IOWA · 1992 · $209,496

## Abstract

Human cytomegalovirus (HCMV) is the major cause of virus-induced
congenital birth defects. It is also a major cause of pneumonitis, which
is frequently fatal in immunocompromised adults. To better understand and
eventually control this pathogen, we propose to continue our
investigation of the genes and gene products that regulate HCMV gene
expression and the cis-acting elements that respond to viral or cellular
factors. This proposal focuses on several different viral gene products
that regulate expression from the major immediate early (IE) enchancer
containing promoter/regulatory region in the large unique component of
the viral genome. These viral gene products are encoded by the tegument
pp65 and/or the tegument pp71, the IE1 and the IE2 genes. The tegument
protein pp65 and the IE1 protein up-regulate expression. In contrast, one
or more of the IE2 proteins down-regulate expression. The IE2
transcription unit codes for a family of viral proteins. The IE2 proteins
and functional domains that down-regulate the major IE
promoter/regulatory region will be investigated. The IE2 proteins also
activate, in trans, inducible viral promoters. IE2 proteins and
functional domains that activate heterologous or homologous early or late
viral promoters will also be investigated. The interaction of these viral
proteins with eukaryotic cell transcription complexes will be
investigated.

The cis-acting elements in the major IE promoter/regulatory region that
respond to cellular and viral transcription factors will be
characterized. The first approach is to clone the viral genes and
determine the effect of wild type or mutant viral proteins on regulation
of the major IE promoter/regulatory region. A second approach is to
identify the cis-acting element(s) by deletion analysis. Since the repeat
elements are interspersed in the promoter/regulatory region, we will also
synthesize each element and analyze its effects independently or in
combination with other elements. The functions of these elements will
then be tested independently or in combination. These experiments should
contribute new information on how the eukaryotic cell and virus-specified
proteins regulate viral gene expression for productive, persistent, or
latent infection.

## Key facts

- **NIH application ID:** 3125486
- **Project number:** 5R01AI013562-17
- **Recipient organization:** UNIVERSITY OF IOWA
- **SAM.gov UEI:** Z1H9VJS8NG16
- **Principal Investigator:** MARK F STINSKI
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1992
- **Award amount:** $209,496
- **Award type:** 5
- **Project period:** 1976-09-01 → 1994-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3125486

## Citation

> US National Institutes of Health, RePORTER application 3125486, REGULATION OF HUMAN CYTOMEGALOVIRUS GENE EXPRESSION (5R01AI013562-17). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3125486. Licensed CC0.

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