Ribonucleic Acid Synthesis in Cells Infected with Herpes Simplex Virus

Ribonucleic Acid Synthesis in Cells Infected with Herpes Simplex Virus I. Patterns of Ribonucleic Acid Synthesis in Productively Infected Cells Edward K. Wagner and Bernard Roizman Department of Microbiology, University of Chicago, Chicago, Illinois 60637 ABSTRACT HEp-2 cells were pulse-labeled at different times after infection with herpes simplex virus, and nuclear ribonucleic acid (RNA) and cytoplasmic RNA were examined. The data showed the following: (i) Analysis by acrylamide gel electrophoresis of cytoplasmic RNA of cells infected at high multiplicities (80 to 200 plaque-forming units (PFU)/cell) revealed that ribosomal RNA (rRNA) synthesis falls to less than 10% of control (uninfected cell) values by 5 hr after infection. The synthesis of 4 S RNA also declined but not as rapidly, and at its lowest level it was still 20% of control values. At lower multiplicities (20 PFU), the rate of inhibition was slower than at high multiplicities. However, at all multiplicities the rates of inhibition of 18 S and 28 S rRNA remained identical and higher than that of 4 S RNA. (ii) Analysis of nuclear RNA of cells infected at high multiplicities by sucrose density gradient centrifugation showed that the synthesis and methylation of 45 S rRNA precursor continued at a reduced but significant rate (ca. 30% of control values) at times after infection when no radioactive uridine was incorporated or could be chased into 28 S and 18 S rRNA. This indicates that the inhibition of rRNA synthesis after herpesvirus infection is a result of two processes: a decrease in the rate of synthesis of 45 S RNA and a decrease in the rate of processing of that 45 S RNA that is synthesized. (iii) Hybridization of nuclear and cytoplasmic RNA of infected cells with herpesvirus DNA revealed that a significant proportion of the total viral RNA in the nucleus has a sedimentation coefficient of 50 S or greater. The sedimentation coefficient of virus-specific RNA associated with cytoplasmic polyribosomes is smaller with a maximum at 16 S to 20 S , but there is some rapidly sedimenting RNA (> 28 S ) here too. (iv) Finally, there was leakage of low-molecular weight (4 S ) RNA from infected cells, the leakage being approximately three-fold that of uninfected cells by approximately 5 hr after infection. Copyright © 1969 American Society for Microbiology CiteULike Connotea Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter What's this? « Previous | Next Article » Table of Contents This Article J. Virol. July 1969 vol. 4 no. 1 36-46 » Abstract PDF Classifications Animal Viruses Services Email this article to a colleague Similar articles in ASM journals Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of JVI Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Load citing article information Citing articles via Web of Science Citing articles via Google Scholar Google Scholar Articles by Wagner, E. K. Articles by Roizman, B. Search for related content PubMed PubMed citation Articles by Wagner, E. K. Articles by Roizman, B. Related Content Load related web page information Social Bookmarking CiteULike Connotea Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter What's this? current issue January 2012, volume 86, issue 1 Spotlights in the Current Issue Two Xenotropic Murine Leukemia Virus Parents Breaking the Entry Targeting Barrier Complex Morphology and Dynamic Development of Poliovirus Membranous Replication Structures Revealed A Staining Artifact Explains Apparent Varicella-Zoster Virus Protein Expression in Neurons Recent Mumps Outbreaks Are Not Caused by Immune Escape Alert me to new issues of JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • [email protected] Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2011 by the American Society for Microbiology. For an alternate route to JVI .asm.org, visit: http://intl- JVI .asm.org | More Info»