# HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO

> **NIH NIH R01** · TUFTS UNIVERSITY BOSTON · 1989 · $208,964

## Abstract

The long term goal of this study is to understand the effect of
Epstein-Barr virus (EBV) infection on the biology of the infected B cell.

1) When EBV infects normal resting B cells it drives them to differentiate
into proliferating lymphoblasts that grow indefinitely.  One major goal of
this study is to understand better the viral functions involved in
activating the B cell with special emphasis on the role of circularization
of the viral genome and expression of the EBV encoded membrane protein p63
(Encoded by the Eco R-1 Dhet fragment of EBV DNA).  To perform this study
we will measure levels of expression of latent viral cellular proteins
(EBNA-1 EBNA-2 and p63) and cellular activation antigens (BLAST-1 and
BLAST-2) in cells infected with intact viral DNA or irradiated DNA that
cannot circularize.  Relative levels of expression of the molecules will be
assessed by immunofluorescence, Northern (RNA) and Western (protein) blots
will also be performed for the viral proteins.  The role of individual
viral gene products will also be assessed by transfecting subgenomic
fragments of EBV DNA into EVB- BL cells and measuring changes in cell
surface phenotype with a battery of B cell specific monoclonal antibodies.

2) In vivo, the infected proliferating B cells are kept in check, in
healthy individuals, by cell mediated immune (CMI) responses.  The target
structure (LYDMA) for CMI remains unknown.  We will test various EBV
encoded proteins (EBNA-1, EBNA-2, p63 and the virion glycoproteins gp
350/220) for their role at targets in CMI.  Target cells that are
autologous or HLA matched to a panel of EBV specific cytotoxic T cell line
(CTL), will be transfected with appropriate fragments of the viral genome.
Expression will be tested by Northern and Western blot analysis and
immunofluorescence.  Successfully transfected cells will then be tested for
their susceptibility to lysis by EBV specific CTL.

The possible role of the only EBV encoded membrane protein in transformed
cells (p63) as LYDMA will also be tested by assessing the ability of
various synthetic peptides, derived from the p63 sequence, to stimulate CTL.

These studies should help us understand at the molecular level, mechanisms
involved when EBV infects and activated B cells and how the healthy immune
response eliminates the infected cells.

## Key facts

- **NIH application ID:** 3128159
- **Project number:** 5R01AI018757-09
- **Recipient organization:** TUFTS UNIVERSITY BOSTON
- **SAM.gov UEI:** C1F5LNUF7W86
- **Principal Investigator:** David A. Thorley-Lawson
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $208,964
- **Award type:** 5
- **Project period:** 1981-09-01 → 1991-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3128159

## Citation

> US National Institutes of Health, RePORTER application 3128159, HOST IMMUNITY TO EBV INFECTION IN VITRO AND IN VIVO (5R01AI018757-09). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3128159. Licensed CC0.

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