The Journal of Experimental Medicine
Torrey Pines Biolabs
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published online 5 March 2001.
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 255K)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ensser, A.
Right arrow Articles by Fleckenstein, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ensser, A.
Right arrow Articles by Fleckenstein, B.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
© The Rockefeller University Press, 0022-1007/2001/3/637/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 5, March 5, 2001 637-642


Brief Definitive Report

Independence of Herpesvirus-induced T Cell Lymphoma from Viral Cyclin D Homologue

Armin Enssera, Diana Glykofrydesa, Henk Niphuisb, Eva M. Kuhnb, Brigitte Rosenwirthb, Jonathan L. Heeneyb, Gerald Niedobitekc, Ingrid Müller-Fleckensteina, and Bernhard Fleckensteina
a Institut für Klinische und Molekulare Virologie der Universität Erlangen-Nürnberg, 91054 Erlangen, Germany
b Biomedical Primate Research Center, Lange, 2288GJ Rijswijk, The Netherlands
c Pathologisch-Anatomisches Institut, 91054 Erlangen, Germany

Correspondence to: Armin Ensser, Institut für Klinische und Molekulare Virologie der Universität Erlangen-Nürnberg, Schlossgarten 4, 91054 Erlangen, Germany. Tel:149-9131-852-3786 Fax:149-9131-852-6493 E-mail:ensser{at}viro.med.uni-erlangen.de.

Cyclin D family members are cellular protooncogenes, and their viral homologues in the Kaposi's sarcoma-associated herpesvirus (KSHV, human herpesvirus type 8 [HHV-8]) and the closely related Herpesvirus saimiri have been implicated as putative cofactors of viral transformation and pathogenesis. KSHV is regularly found in Kaposi's sarcoma and in the primary effusion B cell lymphoma and Castleman's disease associated with immunosuppression and AIDS. H. saimiri strain C488 transforms human and marmoset T cells in vitro and causes polyclonal T cell lymphoma in New World monkeys. The viral cyclins stimulate cell cycle progression of quiescent fibroblasts, and they form active cyclin-dependent kinase (CDK)6 complexes of broad substrate specificity that can resist and downregulate cellular CDK inhibitors. This study shows that the viral cyclin of H. saimiri strain C488 is not required for viral replication, T cell transformation, and pathogenicity in New World primates.

Key Words: cell cycle, gammaherpesviridae, herpesvirus, Kaposi sarcoma associated, oncogenic viruses, callitrichinae


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS