Antibody-dependent enhancement and persistence in macrophages of an arbovirus associated with arthritis.
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 pre-existence of ADE titres was apparent, nor could sera raised against a related arbovirus, Barmah Forest, enhance RRV infection. Tumour necrosis factor-alpha, 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.
Linn
M L
ML
Queensland Institute of Medical Research, Box Royal Brisbane Hospital, Australia.
Aaskov
J G
JG
Suhrbier
A
A
D018354:Alphavirus Infections / Q000821:virology*; D000818:Animals; D019067:Antibody-Dependent Enhancement; D001170:Arthritis, Infectious / Q000821:virology*; D002460:Cell Line; D006801:Humans; D008264:Macrophages / Q000276:immunology / Q000821:virology*; D012398:Ross River virus / Q000276:immunology / Q000502:physiology*; D014779:Virus Replication