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 Docherty, J. J. Articles by Rapp, F. Search for Related Content PubMed PubMed Citation Articles by Docherty, J. J. Articles by Rapp, F. Agricola Articles by Docherty, J. J. Articles by Rapp, F.

Mechanism of the Restricted Growth of Herpes Simplex Virus Type 2 in a Hamster Cell Line

Department of Microbiology, College of Medicine, The Milton S. Hershey Medical Center of The Pennsylvania State University, Hershey, Pennsylvania 17033 U.S.A.

A hamster cell line (HDC-22) developed in our laboratory was non-permissive for herpes simplex virus type 2 (HSV-2) but not for herpes simplex virus type 1 (HSV-1). The mechanism of resistance to productive infection by HSV-2 was investigated. Adsorption studies revealed that HSV-1 and HSV-2 adsorbed at similar rates to the HDC-22 cells. The HDC-22 cells, when infected with HSV-2, produced minimal amounts of virus-specific antigens which increased slightly after several days.

The amount of HSV-2 DNA produced in the HDC-22 cells was always less than when these cells were infected with HSV-1. Cellular DNA synthesis was severely depressed by infection with HSV-1 at a multiplicity of 1 while HSV-2 had no effect at this multiplicity. At a higher multiplicity (of 5), this effect was increased with HSV-1 and noticeable with HSV-2. These studies indicate that the block for infection of the HDC-22 cell line with HSV-2 is after virus adsorption and may involve synthesis of virus DNA.

Received 1 January 1972; accepted 17 April 1972.