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Email ghayward@jhmi.edu
Phone (410) 955-8686

Gary S. Hayward, Ph.D.

Primary Appointment in Oncology and in Pharmacology and Molecular Sciences; Secondary Appointment in Pathology
Member, Graduate Program in Biochemistry, Cellular and Molecular Biology; Member, Graduate Program in Cellular and Molecular Medicine; Member, Graduate Programin Pathobiology; Member, Graduate Program in Pharmacology and Molecular Sciences

Herpes viruses have developed successful genetic strategies that allow them to target to specific cell types or tissues where they can reside temporarily in a quiescent or latent state without damaging the host cell. However, immuno suppression, allograft transplantation and other stress conditions often lead to accelerated reactivation and disseminated spread of lytic or abortive infection with associated serious pathology and disease. The molecular mechanisms used by herpes simplex virus and Epstein Barr virus to establish and reactivate from latency in sensory neurons and immortalized B lymphocytes are now relatively well understood. However, in recent years it has also become apparent that cytomegalovirus (CMV), HHV 6/7 and Kaposi's sarcoma herpes virus (HHV 8) are harbored as widespread latent infections in monocytes, T cells and vascular endothelial cells and can be associated with or causative agents of chronic disease after immunosuppression and organ transplantation. Our group is especially interested in molecular mechanisms involved in herpes virus host cell interactions in vascular tissue and myeloid cells in the settings of cardiac, lung and renal transplants and AIDS. This includes study of the roles of viral encoded angiogenic cytokines and chemokine receptors, effects of viral immediate-early genes on cell cycle regulation and very early events in the nucleus including alterations in subnuclear compartments involving PML and SUMO-modification mechanisms. Potential pathogenic variants of specific viral genes are also being evaluated.

Wu F., Ahn J-H, Alcendor D, Jang W-J, Xiao J, Hayward SD, Hayward GS. OriginIndependent Assembly of Kaposi's Sarcoma-associated Herpesvirus DNAReplication Compartments in Transient Cotransfection Assays and Association with the ORF-K8 Protein and Cellular PML. J. Virol. 75:1487-1506, 2001.

Ciufo DM, Cannon JS, Poole LJ, Wu F, Murray P, Ambinder RF, Hayward GS. Spindle Cell Conversion by Kaposi's Sarcoma-Associated Herpesvirus: Formation of Colonies and Plaques with Mixed Lytic and Latent Gene Expression in Infected Primary Dermal Microvascular Endothelial Cell Cultures. J. Virol.75:5614-5626, 2001.

Poole L., Yu Y, Kim P, Zheng QZ, Pevsner J, Hayward GS. Altered Patternsof Cellular Gene Expression in Dermal Microvascular Endothelial Cells Infected with the Kaposi's Sarcoma Associated Herpesvirus. J. Virol.76:3395-3420, 2002.

Chiou C-J, Poole L, Kim P, Ciufo DM, Cannon JS, ap Rhys CM, Alcendor DJ,Zong J-C, Ambinder RF, Hayward GS. Patterns of Gene Expression and a Transactivation Function Exhibited by the vGCR (ORF 74) Chemokine Receptor Protein of Kaposi's Sarcoma-Associated Herpesvirus. J. Virol. 76:3421-3439,2002.


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