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1 Queensland Institute of Medical Research, Box Royal Brisbane Hospital, Queensland 4029
and2 WHO Collaborating Centre for Arbovirus Reference and Research, School of Life Science, Queensland University of Technology, Brisbane, Queensland 4001, Australia
Ross River virus (RRV) is the aetiological agent of epidemic polyarthritis (EPA) a predominantly rheumatic disease afflicting up to 5000 Australians annually. We show here for the first time that macrophages can be productively infected by RRV. Subneutralizing titres of anti-RRV IgG (but not IgM) also showed classical antibody-dependent enhancement (ADE) of RRV infection in macrophage and monocyte cell lines. No correlation between development of EPA and the preexistence of ADE titres was apparent, nor could sera raised against a related arbovirus, Barmah Forest, enhance RRV infection. Tumour necrosis factor-
, implicated in the immunopathogenesis of rheumatoid arthritis, was not secreted by RRV-infected monocytes or macrophages. Macrophage cell lines infected with RRV were, however, capable of producing virus for over 50 days. RRV-induced arthritis may therefore be due to the persistent productive infection of macrophages, perhaps established by a brief period of ADE early in infection.
* Author for correspondence. Fax +61 7 33620106. e-mail andreasS@qimr.edu.au
Received 22 May 1995;
accepted 13 October 1995.
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