Effect on mice of infection during pregnancy with three Australian arboviruses.

Infection of pregnant mice with Ross River or Getah viruses after the establishment of a functional placenta resulted in fetal infection with these viruses. However, only with Ross River virus was there any significant fetal death. There was significant post-partum mortality in mice infected in utero with Ross River but not with Getah virus. In contrast, significant post-partum mortality occurred in Murray Valley encephalitis virus-infected mice despite the inability of the virus to cross the placenta. Infection of mice with Ross River, Getah, or Murray Valley encephalitis viruses before placentation had occurred (5th day post-conception) did not result in fetal infection although there was significant post-partum death in litters born to Ross River virus-infected mothers.

An epidemic of Ross River virus infection in Fiji, 1979.

An explosive epidemic of polyarthritis caused by Ross River virus occurred in the Fijian islands from April to June 1979. Serological results suggest there was a low level of Alphavirus activity throughout Fiji before April 1979, but that following the epidemic up to 90% of the residents of some communities had antibody to Ross River virus. The clinical and laboratory findings in patients from the Fijian outbreak were similar to those seen in Australian cases.

Regulation in vitro of human natural killer (NK) cell activity.

The natural killer cell activity of PBL from epidemic polyarthritis patients was depressed early after onset of symptoms but returned to normal as the patient recovered. This study found that the in vitro culture of Ross River virus, the agent responsible for epidemic polyarthritis, with PBL resulted in enhanced rather than depressed NK cell activity. Evidence was also obtained that NK cell activity could be suppressed by suppressor-T lymphocytes generated by culture of PBL with high concentrations of Concanavalin A. This suppressive activity was not due to release of a soluble mediator(s) by the suppressor T cells.

Specific and non-specific immunological changes in epidemic polyarthritis patients.

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 or T-lymphocytes from peripheral blood to proliferate on re-exposure to Ross River virus.

Detection by ELISA of IgM antibodies to Ross River virus in serum from patients with suspected epidemic polyarthritis.

An ELISA method for the detection of IgM antibody to Ross River virus in the serum of patients with suspected epidemic polyarthritis has been developed. None of the reagents is infectious or toxic and the use of purified virus minimizes the risk of non-specific reactions to non-viral products. In a positive reaction the ELISA substrate changes colour from yellow to purple, enabling serum antibody titres to be read by eye.

Cell-mediated immune response to Ross River virus in mice: evidence for a defective effector cell response.

Spleen cells recovered from mice during a primary infection with Ross River virus showed a virus-specific proliferative response when challenged in vitro. The majority of the proliferating cells were T-lymphocytes. In contrast, there was little detectable migration inhibition factor production by these spleen cells and little or no virus-specific cytotoxic activity. Sub-cutaneous challenge with virus elicited a weak delayed type hypersensitivity reaction.

Evidence for transplacental transmission of Ross River virus in humans.

Immunoglobulin M antibody to Ross River virus was found in the cord blood of 11 368 children born to mothers who were pregnant during the epidemic of Ross River virus infection in Fiji, in 1979. Since IgM antibody does not normally cross the human placenta, these findings are suggestive of in-utero infection. Antibody to Ross River virus was also present in eight of the 11 mothers of children with IgM-positive cord blood. One of the mothers with IgM-negative blood had no detectable haemagglutination-inhibiting antibody to Ross River virus. All children appeared normal at birth.

Natural killer cells in viral arthritis.

Changes in natural killer (NK) cell activity were studied in patients with polyarthritis associated with rubella or Ross River virus infections. In 30 of 32 Ross River virus patients, peripheral NK cell activity was depressed at some stage of the disease but returned to normal levels as patients recovered from arthritic symptoms. Similar changes did not occur in rubella patients and no difference was found between changes in peripheral NK activity and serum interferon (IFN) levels in rubella patients with arthritis and those without. Neither the peak of NK cell activity in peripheral blood lymphocytes (PBL) recovered early in Ross River virus and rubella infections, nor the depression of NK cell activity late in Ross River virus infections could be correlated with changes in serum IFN levels. The decrease in PBL-NK cell activity in epidemic polyarthritis (EPA) patients could not be attributed solely to loss of NK cells from the peripheral circulation because limiting-cell-dilution (LCD) analyses indicated changes in peripheral NK cell activity were due to changes in both the number and lytic activity of NK cells. Despite the association between HLA-DR7 and EPA no differences were found in levels of peripheral NK cell activity in DR7+ and DR7- EPA patients. The demonstration that peripheral NK cells could kill autologous synovial cells suggested that NK cells in joints of EPA patients may contribute to the arthritis associated with Ross River virus infection.