# STRUCTURE AND FUNCTION OF VARICELLA ZOSTER DNA

> **NIH NIH R01** · STATE UNIVERSITY OF NEW YORK AT BUFFALO · 1992 · $155,120

## Abstract

Varicella zoster virus (VSV) is, by virological standards, one of the most
successful human herpesviruses.  It infects the great majority of the
population in childhood and remains latent in spinal ganglia to reappear as
zoster in aging populations.  While VZV spreads readily and efficiently in
its human host, it is still, despite much effort on the part of
virologists, difficult to handle in the laboratory.  It is the first human
herpesvirus for which a live-attenuated vaccine strain (Oka) has been
licensed in the U.S., but the characteristics of Oka which make it suitable
for use as a vaccine are not understood.  In this proposal, we plan to
address several aspects of VZV gene expression (particularly that of
glycoproteins) in the context both of virus development (or lack of it) in
the infected cell and of the host's immune responses to infection with
wild-type and with vaccine virus.  There are five specific aims.  In the
first of these, we expand on work carried out in the previous granting
period, proposing to develop monoclonal antibodies against gpV as a means
of mapping antigenic sites on this virus-neutralising polypeptide.  In aim
2, we will clone glycoproteins gpII and gpIII into vaccinia expression
systems.  These, along with proteins already cloned (gpV, gpIV, gpI, major
capsid protein, major immediate early protein) will be used in
immunological assays (humoral and cell-mediated) as well as in protection
studies using guinea pig models of VZV infection.  Next, null mutants in
those glycoproteins (gpV, gpIV, gpI) which we know or strongly suspect to
be inessential for growth in cell culture will be constructed; animal model
studies will then be pursued with both single and multiple variants.  In
the fourth aim, the reagents generated above will be used to investigate
the nature and kinetics of association of gpV within infected cell
membranes and its quaternary relationship to other VZV glycoproteins.  Aim
five focusses on our observation that the Oka strain of VZV is markedly
deficient in the expression of gpV; we should like to define this lesion
and attempt to correlate it to the relatively avirulent behavior of the Oka
vaccine strain in vivo.

## Key facts

- **NIH application ID:** 3127953
- **Project number:** 5R01AI018449-12
- **Recipient organization:** STATE UNIVERSITY OF NEW YORK AT BUFFALO
- **SAM.gov UEI:** LMCJKRFW5R81
- **Principal Investigator:** WILLIAM T RUYECHAN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1992
- **Award amount:** $155,120
- **Award type:** 5
- **Project period:** 1982-08-01 → 1995-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3127953

## Citation

> US National Institutes of Health, RePORTER application 3127953, STRUCTURE AND FUNCTION OF VARICELLA ZOSTER DNA (5R01AI018449-12). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3127953. Licensed CC0.

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