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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 regulated by human herpesvirus infections, we studied the gene expression profile of lymphocytes infected with human herpesvirus 6 (HHV-6) by using a novel immunomicroarray. Our nylon-based immunomicroarray contained more than 1,150 immune response-related genes and was highly consistent between experiments. Experimentally, we found that independently of the HHV-6 strain used to infect T cells, multiple proinflammatory genes were increased and anti-inflammatory genes were decreased at the mRNA and protein levels. HHV-6 strains A and B increased expression of the genes for interleukin-18 (IL-18), the IL-2 receptor, members of the tumor necrosis factor alpha superfamily receptors, mitogen-activated protein kinase, and Janus kinase signaling proteins. As reported previously, CD4 protein levels were also increased significantly. Specific type 2 cytokines, including IL-10, its receptor, and IL-14, were downregulated by HHV-6 infection and, interestingly, amyloid precursor proteins and type 1 and 2 presenilins. Thus, T cells respond to HHV-6 infection by inducing a type 1 immune response that may play a significant role in the development and progression of diseases associated with HHV-6, including pediatric, hematologic, transplant, and neurologic disorders.

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

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.


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