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Journal of Virology, March 2000, p. 2612-2619, Vol. 74, No. 6
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Infection of Primary Human Monocytes by Epstein-Barr Virus

Martin Savard,1 Carole Bélanger,1 Mélanie Tardif,1 Pierrette Gourde,1 Louis Flamand,2 and Jean Gosselin1,*

Laboratory of Viral Immunology1 and Laboratory of Virology,2 Centre de Recherche en Rhumatologie et Immunologie, Centre de Recherche du CHUL, Université Laval, Sainte-Foy, Québec, Canada

Received 9 August 1999/Accepted 17 December 1999

Previous studies have reported that infection of monocytes by viruses such as cytomegalovirus and human immunodeficiency virus weakens host natural immunity. In the present study, we demonstrated the capability of Epstein-Barr virus (EBV) to infect and replicate in freshly isolated human monocytes. Using electron microscopy analysis, we observed the presence of EBV virions in the cytoplasm and nuclei of approximately 20% of monocytes. This was confirmed by Southern blot analysis of EBV genomic DNA sequences in isolated nuclei from monocytes. Infection of monocytes by EBV leads to the activation of the replicative cycle. This was supported by the detection of immediate-early lytic mRNA BZLF-1 transcripts, and by the presence of two early lytic transcripts (BALF-2, which appears to function in DNA replication, and BHRF-1, also associated with the replicative cycle). The late lytic BcLF-1 transcripts, which code for the major nucleocapsid protein, were also detected, as well as EBNA-1 transcripts. However, attempts to detect EBNA-2 transcripts have yielded negative results. Viral replication was also confirmed by the release of newly synthesized infectious viral particles in supernatants of EBV-infected monocytes. EBV-infected monocytes were found to have significantly reduced phagocytic activity, as evaluated by the quantification of ingested carboxylated fluoresceinated latex beads. Taken together, our results suggest that EBV infection of monocytes and alteration of their biological functions might represent a new mechanism to disrupt the immune response and promote viral propagation during the early stages of infection.

* Corresponding author. Mailing address: Laboratory of Viral Immunology, Centre de Recherche en Rhumatologie et Immunologie, CHUQ, Pavillon CHUL, Room T 1-49, 2705 boul. Laurier, Sainte-Foy, Québec G1V 4G2, Canada. Phone: (418) 654-2772. Fax: (418) 654-2127. E-mail: jean.gosselin{at}crchul.ulaval.ca.

Journal of Virology, March 2000, p. 2612-2619, Vol. 74, No. 6
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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