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Clinical and Diagnostic Laboratory Immunology, January 2002, p. 19-27, Vol. 9, No. 1
1071-412X/01/$04.00+0     DOI: 10.1128/CDLI.9.1.19-27.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Viral Replication and Host Gene Expression in Alveolar Macrophages Infected with Ebola Virus (Zaire Strain)

Tammy R. Gibb,* David A. Norwood, Jr., Neal Woollen, and Erik A. Henchal

Diagnostic Systems Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland 21702-5011

Received 16 May 2001/ Returned for modification 9 June 2001/ Accepted 4 October 2001

In order to characterize the cellular response to and identify potential diagnostic markers for the early detection of Ebola virus, an in vitro culture system involving nonhuman primate alveolar macrophages was developed. Ebola virus replication in the alveolar macrophages was characterized by plaque assay, immunohistochemical analysis, and in situ hybridization. Fluorogenic 5' -nuclease assays specific for nonhuman primate proinflammatory cytokines and chemokines were designed and used to evaluate mRNA transcription in macrophages infected with Ebola virus. Transient increases in cytokine and chemokine mRNA levels were observed immediately following exposure to Ebola virus. At 2 h postexposure, levels of cytokine and chemokine mRNAs were markedly reduced. Although Ebola virus infection of alveolar macrophages failed to induce a sustained increase in proinflammatory cytokine and chemokine mRNA transcription (potentially reducing the use of these markers as diagnostic tools), the fluorogenic 5'-nuclease assays developed may have prognostic value for individuals infected with Ebola virus. Recently published data have indicated that persons who remain asymptomatic after exposure to Ebola virus are capable of mounting an early proinflammatory cytokine response and that those who become clinically ill are not. If implemented immediately after exposure, these assays could be used to predict which individuals will be more likely to remain asymptomatic as opposed to those who will be more likely to develop clinical signs and eventually succumb to the virus.


* Corresponding author. Mailing address: DSD, USAMRIID, 1425 Porter St., Fort Detrick, MD 21702-5011. Phone: (301) 619-7193. Fax: (301) 619-2492. E-mail: tammy.gibb{at}sbccom.apgea.army.mil.


Clinical and Diagnostic Laboratory Immunology, January 2002, p. 19-27, Vol. 9, No. 1
1071-412X/01/$04.00+0     DOI: 10.1128/CDLI.9.1.19-27.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




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