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Journal of Virology, February 2001, p. 1378-1386, Vol. 75, No. 3
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.3.1378-1386.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Activation of Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Lytic Replication by Human Cytomegalovirus

Jeffrey Vieira,1,* Patricia O'Hearn,1 Louise Kimball,1 Bala Chandran,2 and Lawrence Corey1

Department of Laboratory Medicine, University of Washington, and Program in Infectious Diseases, Fred Hutchinson Cancer Research Center, Seattle, Washington, 98109,1 and Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, Kansas 661602

Received 9 June 2000/Accepted 6 November 2000

The majority of Kaposi's sarcoma-associated herpesvirus (KSHV)-infected cells identified in vivo contain latent KSHV, with lytic replication in only a few percent of cells, as is the case for the cells of Kaposi's sarcoma (KS) lesions. Factors that influence KSHV latent or lytic replication are not well defined. Because persons with KS are often immunosuppressed and susceptible to many infectious agents, including human cytomegalovirus (HCMV), we have investigated the potential for HCMV to influence the replication of KSHV. Important to this work was the construction of a recombinant KSHV, rKSHV.152, expressing the green fluorescent protein (GFP) and neo (conferring resistance to G418). The expression of GFP was a marker of KSHV infection in cells of both epithelial and endothelial origin. The rKSHV.152 virus was used to establish cells, including human fibroblasts (HF), containing only latent KSHV, as demonstrated by latency-associated nuclear antigen expression and Gardella gel analysis. HCMV infection of KSHV latently infected HF activated KSHV lytic replication with the production of infectious KSHV. Dual-color immunofluorescence detected both the KSHV lytic open reading frame 59 protein and the HCMV glycoprotein B in coinfected cells, and UV-inactivated HCMV did not activate the production of infectious KSHV-GFP. In addition, HCMV coinfection increased the production of KSHV from endothelial cells and activated lytic cycle gene expression in keratinocytes. These data demonstrate that HCMV can activate KSHV lytic replication and suggest that HCMV could influence KSHV pathogenesis.

* Corresponding author. Mailing address: Fred Hutchinson Cancer Research Center D3-100, 1100 Fairview Ave. N., Seattle, WA 98109. Phone: (206) 667-6795. Fax: (206) 667-4411. E-mail: vieiraj{at}u.washington.edu.

Journal of Virology, February 2001, p. 1378-1386, Vol. 75, No. 3
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.3.1378-1386.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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