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.
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.
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.
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