Ross River virus has been incriminated in the etiology of many sporadic and epidemic cases of polyarthritis in Australia and the Pacific. Both synovium and synovial exudate fluid recovered from the knee of an epidemic polyarthritis patient showed a predominantly mononuclear leucocyte infiltrate. Infectious virus could not be recovered from the synovial exudate. Functional natural killer cells were detected in the synovial fluid. Their level of cytotoxic activity was similar to that detected in the peripheral circulation.

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Summary T‐lymphocytes from epidemic polyarthritis patients exhibited a virus specific proliferative response when exposed to Ross River virus in vitro. The magnitude of this response was greater than that of lymphocytes from asymptomatic seropositive donors. The natural killer cell activity of peripheral blood mononuclear leucocytes from these patients was depressed early in disease but returned to normal levels as the severity of the symptoms decreased. Although no in vivo role can yet be assigned to natural killer cells in epidemic polyarthritis, changes in their activity appeared to be more closely associated with the presence or absence of disease symptoms than were levels of anti‐viral antibody or the ability of T‐lymphocytes from peripheral blood to proliferate on re‐exposure to Ross River virus.

Summary Ross River virus was isolated from two out of four seronegative scrum samples obtained from epidemic polyarthritis patients in Australia. Virus isolated from each patient was found to be phenotypically diverse. These isolations suggest that previous failure to isolate virus from epidemic polyarthritis patients in this country may have been due to failure to obtain material (serum) from patients early enough in the course of the disease and to the use of relatively insensitive isolation techniques.

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SUMMARYIn the absence of virus-specific antibody, Ross River virus failed to activate either the classical or alternative complement pathways. Instead, it inhibited the cleavage of C3 via both pathways. The virus did not appear to act by disrupting C3bBb complexes or by preventing cleavage of factor B by factor D. Instead Ross River virus was found to interfere with the actual cleavage of C3 by activated factor B (C3bBb) of the alternative pathway and C4b2a of the classical pathway.

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