Antibody-dependent enhancement and persistence in macrophages of an arbovirus associated with arthritis

J Gen Virol. 1996 Mar;77 ( Pt 3):407-11. doi: 10.1099/0022-1317-77-3-407.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alphavirus Infections / virology*
  • Animals
  • Antibody-Dependent Enhancement*
  • Arthritis, Infectious / virology*
  • Cell Line
  • Humans
  • Macrophages / immunology
  • Macrophages / virology*
  • Ross River virus / immunology
  • Ross River virus / physiology*
  • Virus Replication