# EPSTEIN-BARR VIRUS EXPRESSION IN NORMAL HUMAN EPITHELIUM

> **NIH NIH R01** · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · 1990 · $150,425

## Abstract

Identification of the epithelial cell as the cell permissive for EBV
replication in the oropharynx has reordered our perception of EBV
biology.  We will reexamine the phenomena of EBV-induced
growth transformation, persistance and reactivation in the
context of epithelial cell-lymphocyte interactions.  To this end,
our specific aims are:  (1) to determine the relationship between
EBV activation in epithelium and cellular expression of
differentiation antigens; (2) to examine the role of latent EBV
infection in the induction of epithelial hyperproliferation; (3) to
analyses lymphocyte-epithelial cell interactions in the epidermis
with regard to EBV reactivation and intercellular exchange of
virus.

Laboratory and wild-type EBV will be used to infect epithelial
primary explant cultures capable of in vitro differentiation.  To
correlate stage of cell maturation with EBV antigen expression,
we will use monoclonal antibodies to cell differentiation antigens
(keratin, involucrin).  Functional interrelationships between viral
proteins and elements of epithelial cytoskeleton transiently
expressed during cell differentiation will be examined by
immunoelectron microscopy and microinjection.  Expression of
the EBV latent membrane protein, important in cell
transformation, will be examined in epithelium.  Under aim #2,
EBV's ability to induce proliferation of basal epithelial cells in a
manner analogous to B cells immortalization will be examined in
epithelial grafts in nude mice and in hyperplastic epithelial lesions
of the uterine cervix.  Evidence for an etiologic role of EBV in
epithelial proliferation will be obtained by hybridization analysis
for EBV gene products known to induce cell transformation;
analysis of cell clonality using the structure of EBV termini; and
determination of EBV DNA organization in proliferating cells
(integrated, episomal, linear).  In aim #3, the ability of EBV to
reactivate in latently infected B cells in the epidermis will be
analysed by cocultivation of the two cell types and by
cytohybridization to inflammatory infiltrates of the cervix.  The
issue of enogenous spread of EBV by B cells will be further
addressed by analysis of EBV isolates, shed from separate
anatomical sites, for restriction fragment length polymorphisms.

Unlike in lymphocytes, the entire viral cycle - from latency to
replication - is manifest in epithelial cells.  These studies will
provide new information on EBV pathobiology and cell regulation
of the viral gene expression.

## Key facts

- **NIH application ID:** 3177272
- **Project number:** 5R01CA038877-06
- **Recipient organization:** ST. JUDE CHILDREN'S RESEARCH HOSPITAL
- **SAM.gov UEI:** JL4JHE9SDRR3
- **Principal Investigator:** JOHN W SIXBEY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1990
- **Award amount:** $150,425
- **Award type:** 5
- **Project period:** 1984-12-01 → 1991-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3177272

## Citation

> US National Institutes of Health, RePORTER application 3177272, EPSTEIN-BARR VIRUS EXPRESSION IN NORMAL HUMAN EPITHELIUM (5R01CA038877-06). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3177272. Licensed CC0.

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