TY - JOUR
T1 - Infection and replication of herpes simplex virus type 1 in an organotypic epithelial culture system
AU - Visalli, Robert J.
AU - Courtney, Richard J.
AU - Meyers, Craig
N1 - Funding Information:
We thank Lynn Budgeon and Danuta Huber for excellent technical assistance and we thank Sandra K. Weller for generously supplying the ICP6D null HSV-1 mutant. We also thank Michelle A. Ozbun for critically reading the manuscript. This work was supported by American Cancer Society Grant VM-167 (C.M.) and by Public Health Service Research Grants CA64624 (C.M.), CA42460 (R.J.C.), and CA72053 (R.J.C.) from the National Institutes of Health.
PY - 1997/4/14
Y1 - 1997/4/14
N2 - We have used the organotypic culture system as a model to study the initial infectious process and spread of herpes simplex virus type 1 (HSV-1) in fully stratified and differentiated human epithelial tissue. The growth kinetics of HSV-1 were determined in organotypic tissues of human epidermal or ectocervical origin. Concurrently, we followed the spread of HSV-1 by immunostaining thin sections of infected organotypic tissue. After HSV-1 was applied to the top cornified epithelial layer, virus penetrated to the basal layer of replicating epithelium and grew to high titers. The virus was limited in its spread in that not all cells within the tissue had demonstrable infection. A ribonucleotide reductase mutant, ICP6Δ, could infect and replicate in basal layers of the organotypic tissues. However, we found that spread was limited in, and to, the basal cell layer. Peak ICP6Δ titers were 100-fold less than in cultures infected with wild-type HSV-1. Studies of HSV mutants should allow us to further define the role of specific viral genes which are associated with infection and spread in a tissue culture system that mimics the initial portal of entry for certain HSV infections.
AB - We have used the organotypic culture system as a model to study the initial infectious process and spread of herpes simplex virus type 1 (HSV-1) in fully stratified and differentiated human epithelial tissue. The growth kinetics of HSV-1 were determined in organotypic tissues of human epidermal or ectocervical origin. Concurrently, we followed the spread of HSV-1 by immunostaining thin sections of infected organotypic tissue. After HSV-1 was applied to the top cornified epithelial layer, virus penetrated to the basal layer of replicating epithelium and grew to high titers. The virus was limited in its spread in that not all cells within the tissue had demonstrable infection. A ribonucleotide reductase mutant, ICP6Δ, could infect and replicate in basal layers of the organotypic tissues. However, we found that spread was limited in, and to, the basal cell layer. Peak ICP6Δ titers were 100-fold less than in cultures infected with wild-type HSV-1. Studies of HSV mutants should allow us to further define the role of specific viral genes which are associated with infection and spread in a tissue culture system that mimics the initial portal of entry for certain HSV infections.
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U2 - 10.1006/viro.1997.8484
DO - 10.1006/viro.1997.8484
M3 - Article
C2 - 9143279
AN - SCOPUS:0030906208
SN - 0042-6822
VL - 230
SP - 236
EP - 243
JO - Virology
JF - Virology
IS - 2
ER -