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[Cancer Research 50, 7852-7857, December 15, 1990]
© 1990 American Association for Cancer Research

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Effect of Hexamethylene Bisacetamide and Cyclosporin A on Recovery of Herpes Simplex Virus Type 2 from the in Vitro Model of Latency in a Human Neuroblastoma Cell Line1

Yasuo Kondo, Yoshiaki Yura, Hiroki Iga, Tetsuo Yanagawa, Hideo Yoshida, Nanayo Furumoto and Mitsunobu Sato2

Second Department of Oral and Maxillofacial Surgery [Y. K., Y. Y., H. I., T. Y., H. Y., M. S.], Tokushima University School of Dentistry, 3 Kuramoto-cho, and Tokushima Bunri University [N. F.], Yamashiro-cho Tokushima 770, Japan

The goal of the present work was to examine whether hexamethylene bisacetamide (HMBA) and cyclosporin A affect the recovery of herpes simplex virus type 2 (HSV-2) from an in vitro model of HSV-2 latency in human neuroblastoma cell line IMR-32. IMR-32 cells were infected with HSV-2 at a multiplicity of infection of 0.1 plaque-forming units/cell and were cultured at 40°C for 14 days, resulting in the establishment of a model of HSV-2 latency in IMR-32 cells. When the cultivation temperature was shifted down from 40 to 37°C, recovery of virus growth began to occur after an incubation period of 2 days. During the time of shift-down of the incubation temperature, the latently infected cells were further cultured at 37°C in the presence or absence of 5 mM HMBA or 0.5 µg/ml cyclosporin A, which does not affect stability of HSV-2 nor proliferation of IMR-32 cells. Consequently, the rate of HSV-2 recovery from the latently infected cells cultured in the presence of 5 mM HMBA was significantly increased, as compared with the untreated controls. In addition, the DNA methylation level of the latently infected IMR-32 cells cultured in the presence of HMBA was significantly decreased when compared to the level in the untreated controls. On the other hand, the cultivation of the latently infected cells in the presence of 0.5 µg/ml cyclosporin A resulted in a significant decrease in the rate of HSV-2 recovery. These findings indicate that the recovery of HSV-2 from the model of latency in IMR-32 cells is enhanced by HMBA treatment, which induces a significant decrease of total genomic DNA methylation level, and is inhibited by cyclosporin A treatment.

1 This investigation was supported in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture of Japan.

2 To whom requests for reprints should be addressed.

Received 6/ 4/90. Accepted 9/ 4/90.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1990 by the American Association for Cancer Research.