# LATENCY IN HERPESVIRUS INFECTIONS OF CELLS & TISSUES

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 1992 · $553,391

## Abstract

Herpesviruses are ubiquitous and continue to be responsible for significant
morbidity and mortality in the human population.  In addition, with the
increasing incidence of syndromes in which immunosuppression represents a
base, there is a corresponding increase in numbers of clinically
significant herpesvirus infections.  The long-term objective of this
proposal is a neurovirulence, and neuroinvasiveness--knowledge that is
fundamental to design of methods for control of these agents.  Although the
primary interest is in Herpes simplex type I (HSV-I), studies presented.
With respect to HSV-I, a molecular and functional analysis of the latent
phase transcription units facilitate viral reactivation, and a definition
of other viral genes functioning in reactivation is also sought.
Comparative studies will be concerned with HSV-II and PrV.  Investigations
of CMV (initially murine, and then human) will focus on identifying
latently.  Infected cells and defining viral transcription in these cells.

These aims will be accomplished in experimental animals (principally mice
and rabbits), and will involve the application of contemporary molecular
biological approaches coupled with more traditional virologic and
experimental pathologic methods.  In studies of HSV neuroinvasiveness and
latency, animals will be inoculated on rear footpads, and lumbosacral
spinal ganglia will be the organs of particular interest.  Viral
reactivation studies will employ the rabbit cornea-epinephrine model.
Cytomegalovirus will be studied principally in murine spleens after
parenteral inoculation.  When a foundation has been established in the
model, investigations of appropriate human autopsy-derived material will
follow.  Of particular importance with respect to methods will be those
concerned with 1) the generation and application of HSV-1 recombinants with
various inserts and deletions in the genomic region encoding the latency
associated transcription unit, 2) biological analysis of viral genes
involved in neuroinvasiveness and neurovirulence, and 3) technologies for
development of a more readily investigated "reactivation system" than the
rabbit cornea model presently serving as the base for study.  In all
systems, continued application of in situ hybridization technologies to
identify involved cells and viral transcripts will be employed.

## Key facts

- **NIH application ID:** 3124282
- **Project number:** 5R01AI006246-28
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **SAM.gov UEI:** RN64EPNH8JC6
- **Principal Investigator:** JACK G STEVENS
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1992
- **Award amount:** $553,391
- **Award type:** 5
- **Project period:** 1978-11-01 → 1995-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3124282

## Citation

> US National Institutes of Health, RePORTER application 3124282, LATENCY IN HERPESVIRUS INFECTIONS OF CELLS & TISSUES (5R01AI006246-28). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3124282. Licensed CC0.

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