Chapter 18. Redirecting the Tropism of HSV-1 for Gene Therapy Applications

  1. David T. Curiel M.D. and
  2. Joanne T. Douglas Ph.D.
  1. Qing Bai Ph.D.1,
  2. Edward A. Burton M.D., Ph.D.2,
  3. William F. Goins Ph.D.1 and
  4. Joseph C. Glorioso Ph.D.1

Published Online: 31 MAR 2003

DOI: 10.1002/0471234303.ch18

Vector Targeting for Therapeutic Gene Delivery

Vector Targeting for Therapeutic Gene Delivery

How to Cite

Bai, Q., Burton, E. A., Goins, W. F. and Glorioso, J. C. (2002) Redirecting the Tropism of HSV-1 for Gene Therapy Applications, in Vector Targeting for Therapeutic Gene Delivery (eds D. T. Curiel and J. T. Douglas), John Wiley & Sons, Inc., Hoboken, NJ, USA. doi: 10.1002/0471234303.ch18

Editor Information

  1. Division of Human Gene Therapy, Departments of Medicine, Pathology and Surgery, and the Gene Therapy Center, The University of Alabama at Birmingham, USA

Author Information

  1. 1

    Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA

  2. 2

    Department of Clinical Neurology, University of Oxford, Oxford, England

Publication History

  1. Published Online: 31 MAR 2003
  2. Published Print: 9 AUG 2002

ISBN Information

Print ISBN: 9780471434795

Online ISBN: 9780471234302

SEARCH

Keywords:

  • herpes simplex;
  • gene therapy;
  • glycoprotein D;
  • glycoprotein C;
  • glycoprotein B;
  • adsorption;
  • fusion;
  • endosome;
  • adapter;
  • HveA;
  • HveC;
  • nectin 1

Summary

Herpes Simplex virus (HSV) is a neurotropic DNA virus. Replication-defective HSV particles have many favorable properties as gene therapy vectors, including non-pathogenicity, large capacity for the insertion of transgenes, high infectivity, straightforward production of uncontaminated high-titre stocks, and a latent life cycle in which the virus remains within neurons for the lifetime of the host. Modifying the tropism of HSV might further enhance the utility of this vector system, by dictating the cellular targets of the disabled particles. In this chapter, we examine the mechanisms whereby HSV enters cells and discuss ways in which the relevant processes might be rationally manipulated in order to effect targeted viral delivery of therapeutic transgenes.