TY - JOUR
T1 - Replication and interaction of herpes simplex virus and human papillomavirus in differentiating host epithelial tissue
AU - Meyers, Craig
AU - Andreansky, Samita S.
AU - Courtney, Richard J.
N1 - Funding Information:
This work was supported by National Cancer Institute Grants RO1 CA79006 (C.M.) and RO1 CA42460 (R.J.C) and by the American Cancer Society Grant PF-98-162-01-MB (S.S.A.). Funding was also received from the PA Department of Health, Health Research Formula Funding Program as a part of the PA Tobacco Settlement Legislation, and a Penn State Cancer Research Institute Grant of the Penn State College of Medicine.
PY - 2003/10/10
Y1 - 2003/10/10
N2 - We have investigated the interactions and consequences of superinfecting and coreplication of human papillomavirus (HPV) and herpes simplex virus (HSV) in human epithelial organotypic (raft) culture tissues. In HPV-positive tissues, HSV infection and replication induced significant cytopathic effects (CPE), but the tissues were able to recover and maintain a certain degree of tissue integrity and architecture. HPV31b not only maintained the episomal state of its genomic DNA but also maintained its genomic copy number even during times of extensive HSV-induced CPE. E2 transcripts encoded by HPV31b were undetectable even though HPV31b replication was maintained in HSV- infected raft tissues. Expression of HPV31b oncogenes (E6 and E7) was also repressed but to a lesser degree than was E2 expression. The extent of CPE induced by HSV is dependent on the magnitude of HPV replication and gene expression at the time of HSV infection. During active HSV infection, HPV maintains its genomic copy number even though genes required for its replication were repressed. These studies provide new insight into the complex interaction between two common human sexually transmitted viruses in an in vitro system, modeling their natural host tissue in vivo.
AB - We have investigated the interactions and consequences of superinfecting and coreplication of human papillomavirus (HPV) and herpes simplex virus (HSV) in human epithelial organotypic (raft) culture tissues. In HPV-positive tissues, HSV infection and replication induced significant cytopathic effects (CPE), but the tissues were able to recover and maintain a certain degree of tissue integrity and architecture. HPV31b not only maintained the episomal state of its genomic DNA but also maintained its genomic copy number even during times of extensive HSV-induced CPE. E2 transcripts encoded by HPV31b were undetectable even though HPV31b replication was maintained in HSV- infected raft tissues. Expression of HPV31b oncogenes (E6 and E7) was also repressed but to a lesser degree than was E2 expression. The extent of CPE induced by HSV is dependent on the magnitude of HPV replication and gene expression at the time of HSV infection. During active HSV infection, HPV maintains its genomic copy number even though genes required for its replication were repressed. These studies provide new insight into the complex interaction between two common human sexually transmitted viruses in an in vitro system, modeling their natural host tissue in vivo.
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U2 - 10.1016/S0042-6822(03)00466-5
DO - 10.1016/S0042-6822(03)00466-5
M3 - Article
C2 - 14592758
AN - SCOPUS:0242268375
SN - 0042-6822
VL - 315
SP - 43
EP - 55
JO - Virology
JF - Virology
IS - 1
ER -