HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Stenberg, R. Articles by Pizer, L. Search for Related Content PubMed PubMed Citation Articles by Stenberg, R. Articles by Pizer, L. Agricola Articles by Stenberg, R. Articles by Pizer, L.

Modulation of Herpes Simplex Virus Replication in Adenovirus Transformed Cells

David Spector

Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19174, U.S.A.

The ability of herpes simplex virus type 1 to replicate in cells transformed by adenovirus type 5 is strongly dependent on the origin of the cells. Studies show that adenovirus transformed rat cells lose their permissiveness while cells of hamster or human origin retain their ability to replicate HSV although at a reduced level when compared to the untransformed parent cells. One line of adenovirus transformed rat cells, 107, demonstrates thermosensitive events, allowing HSV to replicate at 34 °C but not at 37 °C. Analysis of the biochemical events taking place at 37 °C showed that virus-specific DNA synthesis was greatly reduced but that all of the late virus structural proteins could be observed after SDS-polyacrylamide gel electrophoresis. It was also demonstrated that shut-off of host macromolecular synthesis appeared to be less efficient after HSV infection of 107 cells than after infection of more permissive cells such as the non-transformed REF line. Collectively the data show that interactions between HSV and the host cell are perturbed when the cell is transformed by type 5 adenovirus. The degree of perturbation ranges from a slight reduction in number of progeny to a completely abortive infection.

^* Present address: Department of Microbiology and Immunology, University of Colorado Medical Center, Denver, Colorado 80262, U.S.A.

Present address: Department of Pathology, Washington, University School of Medicine, St Louis, Missouri 63110, U.S.A.

Received 30 August 1978; accepted 12 January 1979.