Gene Expression Profile of Herpesvirus-Infected T Cells Obtained Using Immunomicroarrays: Induction of Proinflammatory Mechanisms

doi:10.1128/JVI.75.23.11641-11650.2001

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Journal of Virology, December 2001, p. 11641-11650, Vol. 75, No. 23
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.23.11641-11650.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Gene Expression Profile of Herpesvirus-Infected T Cells Obtained Using Immunomicroarrays: Induction of Proinflammatory Mechanisms

Michael Mayne,¹^,^* Chris Cheadle,² Samantha S. Soldan,³^,⁴ Claudio Cermelli,³^,⁵ Yoshihisa Yamano,³ Nahid Akhyani,³ Jim E. Nagel,² Dennis D. Taub,² Kevin G. Becker,² and Steven Jacobson³

Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada¹; Microarray Unit, National Institute on Aging, National Institutes of Health, Baltimore,² and Viral Immunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda,³ Maryland; Institute of Biomedical Sciences, Department of Genetics, George Washington University, Washington, D.C.⁴; and Department of Hygiene, Microbiology and Biostatistics, University of Modena and Reggio Emilia, Modena, Italy⁵

Received 25 May 2001/Accepted 28 August 2001

Herpesvirus infections can frequently lead to acute inflammation, yet the mechanisms regulating this event remain poorly understood.In order to determine some of the immunological mechanisms regulatedby human herpesvirus infections, we studied the gene expressionprofile of lymphocytes infected with human herpesvirus 6 (HHV-6)by using a novel immunomicroarray. Our nylon-based immunomicroarraycontained more than 1,150 immune response-related genes and washighly consistent between experiments. Experimentally, we foundthat independently of the HHV-6 strain used to infect T cells,multiple proinflammatory genes were increased and anti-inflammatorygenes were decreased at the mRNA and protein levels. HHV-6 strainsA and B increased expression of the genes for interleukin-18 (IL-18),the IL-2 receptor, members of the tumor necrosis factor alphasuperfamily receptors, mitogen-activated protein kinase, and Januskinase signaling proteins. As reported previously, CD4 proteinlevels were also increased significantly. Specific type 2 cytokines,including IL-10, its receptor, and IL-14, were downregulated byHHV-6 infection and, interestingly, amyloid precursor proteinsand type 1 and 2 presenilins. Thus, T cells respond to HHV-6 infectionby inducing a type 1 immune response that may play a significantrole in the development and progression of diseases associatedwith HHV-6, including pediatric, hematologic, transplant, andneurologicdisorders.

^* Corresponding author. Mailing address: Department of Pharmacology and Therapeutics, University of Manitoba, R4050 St. BonifaceHospital Research Centre, Winnipeg, Manitoba, Canada R2H 2A6.Phone: (204) 235-3942. Fax: (204) 237-4092. E-mail: mmayne{at}cc.umanitoba.ca.

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