Herpes Simplex Virus Latency: Adaptation to the Peripheral Nervous System. I

Abstract

Herpes simplex virus type 1 (HSV-1) is well adapted to its human host, in which it establishes clinically silent long-term latent infection punctuated by intermittent reactivation. To achieve this, HSV-1 has evolved a complex strategy in which the particular character of its interaction with certain host cells assures its continued persistence and spread in the human community. This review focuses on the biological behavior of the virus as it relates to the acquisition, maintenance, and reactivation of latent infection, concentrating on how HSV-1 infection of individual cell types contributes to the ecology of the virus. Because the molecular biology of HSV-1 replication and the immunology of HSV-1 infections are reviewed in companion articles in this series (1,2), these subjects are considered only briefly as they pertain directly to the issue of latency. This survey follows the author's particular interests and may underemphasize certain aspects of HSV-1 latency which other investigators judge of greater importance. Fortunately, a number of fine reviews of this subject, reflecting divergent viewpoints, are available (3-8).