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

This Article Full Text Full Text (PDF) Raw microarray data Alert me when this article is cited Alert me if a correction is posted Citation Map 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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Bryan, B. A. Articles by Akula, S. M. Search for Related Content PubMed PubMed Citation Articles by Bryan, B. A. Articles by Akula, S. M. Agricola Articles by Bryan, B. A. Articles by Akula, S. M.

Identifying cellular genes crucial for the reactivation of Kaposi's sarcoma-associated herpesvirus latency

Benjaman A. Bryan

Ossie F. Dyson

Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27834, USA

Correspondence
Shaw M. Akula
akulas{at}mail.ecu.edu

Kaposi's sarcoma-associated herpesvirus (KSHV) is the latest addition to the long list of human herpesviruses. Reactivation of latent herpesvirus infections is still a mystery. It was demonstrated recently that the phorbol ester TPA was efficient in inducing a reactivation of KSHV infection in the S phase of the cell cycle. In the present study, flow cytometry-sorted, TPA-induced, KSHV-infected haematopoietic cells (BCBL-1) were used to analyse the expression profiles of cancer-related cellular genes in the S phase of the cell cycle compared with the G0/1 phase by using microarrays. Overall, the S phase of the cell cycle seems to provide KSHV with an apt environment for a productive lytic cycle of infection. The apt conditions include cellular signalling that promotes survivability, DNA replication and lipid metabolism, while blocking cell-cycle progression to M phase. Some of the important genes that were overexpressed during the S phase of the cell cycle compared with the G0/1 phase of TPA-induced BCBL-1 cells are v-myb myeloblastosis (MYBL2), protein kinase-membrane associated tyrosine/threonine 1 (PKMYT1), ribonucleotide reductase M1 polypeptide (RRM1) and peroxisome proliferator-activated receptors delta (PPARD). Inhibition of PKMYT1 expression by the use of specific short interfering RNAs significantly lowered the TPA-induced KSHV lytic cycle of infection. The significance of these and other genes in the reactivation of KSHV is discussed in the following report. Taken together, a flow cytometry–microarray-based method to study the cellular conditions critical for the reactivation of KSHV infection is reported here for the first time.

An Excel spreadsheet showing raw microarray data for one representative trial is available as supplementary material in JGV Online.

These authors contributed equally to this work.

This article has been cited by other articles:

				A. G. Whitman, O. F. Dyson, P. J. Lambert, T. L. Oxendine, P. W. Ford, and S. M. Akula Changes occurring on the cell surface during KSHV reactivation J. Electron Microsc. (Tokyo), January 1, 2007; 56(1): 27 - 36. [Abstract] [Full Text] [PDF]

				P. W. Ford, B. A. Bryan, O. F. Dyson, D. A. Weidner, V. Chintalgattu, and S. M. Akula Raf/MEK/ERK signalling triggers reactivation of Kaposi's sarcoma-associated herpesvirus latency. J. Gen. Virol., May 1, 2006; 87(Pt 5): 1139 - 1144. [Abstract] [Full Text] [PDF]