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Journal of Virology, June 2000, p. 5190-5197, Vol. 74, No. 11
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Involvement of the Mannose Receptor in Infection of Macrophages by Influenza Virus

Patrick C. Reading,dagger Joanna L. Miller, and E. Margot Anders*

Department of Microbiology and Immunology, University of Melbourne, Parkville, Victoria 3052, Australia

Received 4 October 1999/Accepted 1 March 2000

Influenza viruses A/PR/8/34 (PR8; H1N1), A/Aichi/68 X-31 (HKx31; H3N2), and A/Beijing/89 X-109 (BJx109; H3N2) show marked differences in their ability to infect murine macrophages, including resident alveolar and peritoneal macrophages as well as the macrophage-derived cell line J774. The hierarchy in infectivity of the viruses (PR8 < HKx31 < BJx109) resembles that of their reactivity with mannose-binding lectins of the collectin family. Since the macrophage mannose receptor recognizes the same spectrum of monosaccharides as the collectins do, we investigated the possible involvement of this receptor in infection of macrophages by influenza virus. In competitive binding studies, the binding of 125I-labeled mannosylated bovine serum albumin to macrophages was inhibited by the purified hemagglutinin and neuraminidase (HANA) glycoproteins of influenza virus but not by HANA that had been treated with periodate to oxidize its oligosaccharide side chains. The inhibitory activity of HANA from the three strains of virus differed markedly and correlated with the infectivity of each virus for macrophages. Infection of macrophages, but not MDCK cells, by influenza virus was inhibited by yeast mannan. A variant line of J774 cells, J774E, which expresses elevated levels of the mannose receptor, was more readily infected than J774, and the sensitivity of J774E cells to infection was greatly reduced by culture in the presence of D-mannose, which down-modulated mannose receptor expression. Together, the data implicate the mannose receptor as a major endocytic receptor in the infectious entry of influenza virus, and perhaps other enveloped viruses, into murine macrophages.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Melbourne, Grattan St., Parkville, Victoria 3052 Australia. Phone: 61 3 9344 5702. Fax: 61 3 9347 1540. E-mail: m.anders{at}microbiology.unimelb.edu.au.

dagger Present address: Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom.

Journal of Virology, June 2000, p. 5190-5197, Vol. 74, No. 11
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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