# THE MECHANISM OF VIRUS INDUCED CELL FUSION

> **NIH NIH R01** · PENNSYLVANIA STATE UNIVERSITY, THE · 1987 · $90,128

## Abstract

Mutants of HSV-1 that cause extensive fusion during a productive infection
have been physically mapped to the prototypic genome coordinates 0.732 to
0.753.  One of these mutations in MP, as well as a second mutation that
regulates the production of glycoprotein gC, has been located within the
coding sequences of ICP-27.  Experiments are proposed to study fusion
produced by mutational changes in this region.  Linker mutagenesis (XbaI
and perhaps BclI) at random sites throughout the cloned DNA of this region
will provide for rapid and accurate location of the linker after its
transfer to KOS DNA.  Base substitution mutagenesis will also be employed.
Linker mutagenesis may also increase the speed with which DNA sequence
analysis of the mutants may be determined.  Suppressor mutations of fusion
throughout the HSV-1 genome (using cloned EcoRI fragments) will also be
produced and located.  The production of gC by the presence and absence of
ICP-27 in cis and trans will be determined.  These regulatory studies, as
well as those that locate target sequences in gB (a fusion-inducing gene
adjacent to ICP-27) for fusion by the gene X and ICP-27 products, will
employ an HSV-1/prokaryotic shuttle-vector that forms defective virus
particles in the presence of a helper virus.  A map of the target sequences
within gB, the primary HSV-1 molecule possessing fusion activity, for
syncytium formation by gene X and ICP-27 gene products will employ deletion
mapping of gB.  gB deletion, gene X (or ICP-27) syncytium-inducing viruses
will be incubated with a shuttle vector that contains cloned gB genes with
short deletions at random sites throughout the gB coding sequences and
assayed for fusion during infection on nonpermissive cells.  The gene X
product will be obtained by expression of the HSV-1 peptides in a
tripartite plasmid in E. coli.  Antibodies produced against the tripartite
protein will be used to precipitate the gene X product from infected cells
in order to characterize its fusion-inducing role.

## Key facts

- **NIH application ID:** 3124969
- **Project number:** 5R01AI011513-14
- **Recipient organization:** PENNSYLVANIA STATE UNIVERSITY, THE
- **SAM.gov UEI:** NPM2J7MSCF61
- **Principal Investigator:** STANLEY PERSON
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $90,128
- **Award type:** 5
- **Project period:** 1977-07-01 → 1988-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3124969

## Citation

> US National Institutes of Health, RePORTER application 3124969, THE MECHANISM OF VIRUS INDUCED CELL FUSION (5R01AI011513-14). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3124969. Licensed CC0.

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