J Gen Virol Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Gen Virol 68 (1987), 1749-1753; DOI 10.1099/0022-1317-68-6-1749
© 1987 Society for General Microbiology

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Krilov, L. R.
Right arrow Articles by McIntosh, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Krilov, L. R.
Right arrow Articles by McIntosh, K.
Agricola
Right arrow Articles by Krilov, L. R.
Right arrow Articles by McIntosh, K.

Respiratory Virus Infection of Peripheral Blood Monocytes: Correlation with Ageing of Cells and Interferon Production in vitro

Leonard R. Krilov1, R. Michael Hendry2,{dagger}, Ellen Godfrey2 and Kenneth McIntosh2

1 Division of Infectious Diseases, Schneider Children's Hospital of Long Island Jewish Medical Center, New Hyde Park, New York 11042 and State University of New York at Stony Brook, Stony Brook, New York 11794
and2 Division of Infectious Diseases, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, U.S.A.

The ability of respiratory syncytial virus (RSV) and parainfluenza virus type 3 (PIV3) to replicate in peripheral blood monocytes cultured in vitro for 1, 2, 4 or 7 days prior to infection was investigated. Inoculation of 1-day old monocytes produced at least tenfold less new virus than infection of the older, more macrophage-like cells for both viruses. PIV3 induced extensive syncytium formation, whereas RSV caused a cytopathic effect manifest by increased rounding of the cells with minimal syncytium formation. Supernatants of infected monocytes were assayed for human interferon-{alpha} (HuIFN-{alpha}) in an attempt to explain the restricted viral replication in the youngest monocytes. In PIV3-infected cells, HuIFN-{alpha} production was inversely correlated with new virus formation. Monocytes infected after 1 day in culture produced 800 IU/ml of HuIFN-{alpha}; the older cells produced 100 to 200 IU/ml. In contrast, monocytes infected on day 1 with RSV produced minimal amounts (1.5 IU/ml) of HuIFN-{alpha}. Increasing amounts of HuIFN-{alpha} were detected in cells infected with RSV after 2, 4 or 7 days in culture, reaching a maximum of 400 IU/ml on day 7. Further investigation of the apparent restriction of replication in young monocyte cultures may be helpful in understanding the pathogenesis of these respiratory infections.

Keywords: RS virus, PIV3, monocytes, interferon (HuIFN-{alpha})

{dagger} Present address: Division of Virology, Office of Biologics, Food and Drug Administration, Bethesda, Maryland 20205, U.S.A.

Received 11 November 1986; accepted 18 March 1987.


This article has been cited by other articles:


Home page
J. Virol.Home page
Y.-C. Chen and S.-Y. Wang
Activation of Terminally Differentiated Human Monocytes/Macrophages by Dengue Virus: Productive Infection, Hierarchical Production of Innate Cytokines and Chemokines, and the Synergistic Effect of Lipopolysaccharide
J. Virol., August 28, 2002; 76(19): 9877 - 9887.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
J. Kutza, L. Crim, S. Feldman, M. P. Hayes, M. Gruber, J. Beeler, and K. A. Clouse
Macrophage Colony-Stimulating Factor Antagonists Inhibit Replication of HIV-1 in Human Macrophages
J. Immunol., May 1, 2000; 164(9): 4955 - 4960.
[Abstract] [Full Text] [PDF]


Home page
Clin. Microbiol. Rev.Home page
J. B. Domachowske and H. F. Rosenberg
Respiratory Syncytial Virus Infection: Immune Response, Immunopathogenesis, and Treatment
Clin. Microbiol. Rev., April 1, 1999; 12(2): 298 - 309.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 1987 by the Society for General Microbiology.