ABSTRACT
An exoerimental model of enterically transmitted non-A, non-B hapatitis was established in rhesus and cynomolgus monkeys (Macaca mulatta and Macaca fascicularis). Two monkeys previously infected with 10 per cent pooled stool suspensions of Myanmar patients with well-defined enterically transmitted non-A, non-B, hepatitis and three virgin control monkeys were infected simultaneously with pools of stool suspensions from the first-passage. None of the two previously infected monkeys developed signs of hepatitis. All the control virgin monkeys exhibited hepattis as evident by sharp rise in serum aminotransfrases and pathological changes of acute hepatitis in liver biopsies. These findings document the establishment of immunity after infection with enterically transmitted non-A, non-B hepatitis virus in rhesus and cynomolgus monkeys.
ABSTRACT
The survival period of BALB/c nu/nu mice after Plasmodium berghei NK65 infection was significantly longer than the BALB/c nu/+ mice after an infection with the same parasite. No such difference was found after infection with the same parasite. No such difference was found after infection with Plasmodium yoelli 17x. The difference in the survival perdio was not due to the difference in parasitaemia level. Studies of several immunological parameters revealed that the mice that survived longer showed an increased ability to generate interleukin-2 (IL2) and cytotoxic T lympocytes (CTL) from their spleen cells. We had reported that the survival period had no relationship with the amount of antimalarial antibody production nor the formation of immune complexes(1). T cell functions were found to be generally decreased and natural killer (NK) cell activity was raised in all the mice regardless of their different survival periods. Our experiments suggested the contribution of ILT in the clinical outcome of a malarial infection.
Subject(s)
MalariaABSTRACT
Poasmodium berghei NK 65 or Plasmodium yoelii (lethal strain)was inoculated into normal BALB/c mice, BALB/c nu/nu mice, neonatally thymectomized mice (NTx) and antithymocyte serum treated neonatally thymectomized mice (NTx + ATS). Periods of survival were compared to one another. The nu/nu, NTx and NTx + ATS mice survived significantly longer than normal BALB/c mice P. berghei infection, whereas no such difference was noticed after P. yoelii infection. Antimalarial antibodies and circulating immune complex (CIC) levels were measured in order to examine their correlation with the survival period. A significant difference in the state of equilibrium between antibodies and CICs was revealed. Most of the antibodies induced by P. yoelii formed CICs whereas a portion of the antibodies induced by P. berghei remained unbound. However, no correlation between mortality pattern and serological changes was found. Therefore it seems unlikely that antimalarial antibodies and CICs are harmful factors responsible for the earlier death of the immunocompetent mice.