THE ROLE OF CELLULAR AND HUMORAL IMMUNITY IN THE PATHOGENESIS OF EXPERIMENTAL PlCHINDE VIRUS INFECTION IN MICE
THE ROLE OF CELLULAR AND HUMORAL IMMUNITY IN THE PATHOGENESIS OF EXPERIMENTAL PlCHINDE VIRUS INFECTION IN MICE
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Date
1983-11
Authors
AHMAD, Aliyu
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Abstract
The role of cell mediated and humeral immune response in the pathogenesis of experimental pitchblende virus infection in CAB mice was investigated. The study showed, that cell mediated immunity as measured by introit 51 T lymphocyte mediated Sisely of cr-labelled target L cells played a vital role in the pathogenesis of acute lethal pitchblende virus infection of suckling CAB nice. During the period of maximum Sisely (8-9 days post infection) clinical symptoms were apparent in the acutely infected mice, at the sane time histopathological changes consisting of inflammatory cell infiltrations and necrosis of vital, organs such as the liver, kidneys and brain were prominent removal of T lymphocytes by antithetical serum resulted in considerable reduction of mortality while depletion oi macrophages or B lymphocytes did not significantly reduce mortality or cytotoxic. Adoptive transfer of immune lymphocytes, best obtained from synergistic pitchblende virus infected mice to persistent pitchblende virus carrier mice also resulted in mortality. While humeral immunity did not contribute significantly to the pathogenesis of acute pitchblende virus infection of suckling CBA mice neither did antibody dependent cell mediated cytotoxicity play a significant role in the pathogenesis of the infection. It was observed that in persistently infected pichinde virus carrier CBA mice, antibody played a vital role in the pathogenesis of pichinde virus infection as these persistent pichinde virus carrier mice
iv. developed circulating immune complexes which gradually deposited in the kidneys of the carrier mice and contributed to glomerulonephritis, fibrinoid necrosis and perivascular inflammations which resulted ultimately to the death of most of the carrier mice. Removal of virus -antivirus immune complexes from the sera of these carrier nice by precipitation with anti mouse gamma globulin resulted in significant reduction of infectivity. Although it was shown in this dy that H-2 identity between the effector and target cells would yield maximum lysis of pinochle virus infected target cells, there was no significant difference in susceptibility of the four inbred strains of mice ering in H-2 haplotype to acute pitchblende virus infection is all the inbred strains were equally susceptible to lethal pic hind e virus infection. This study also revealed that mononuclear cells from CBA mice either acutely or persistently infected with pichinde virus yield infectious virus when measured by infectious centre assay though the yield from acutely infected mice was higher than the yield from persistent carriers, furthermore mitogenic stimulation of these cells gave increased levels of infectious centre forma-tion which might suggest that these cells might serve as reservoir for virus persistency.
v. Striking differences between the immune phenomena, pathology and clinical manifestations of pitchblende virus infection and the type or model arena virus disease lymphocytic choriomeningitis (LCM) were observed. The expirations, which may be in age, strain and aex-dependent regulatory factors , may be very important in finding a Key to prophylaxis or therapy in the arena virus - caused human diseases which include the type disease LCM and also Lassa fever, endemic in Nigeria. Future studies will be oriented in this direction.
Description
A thesis submitted Department of science,faculty of pharmaceutical science,Ahmadu Bello university Zaria.Nigeria November 1983.
Keywords
ROLE,, CELLULAR,, HUMORAL,, IMMUNITY,, PATHOGENESIS,, EXPERIMENTAL,, PlCHINDE VIRUS, INFECTION IN MICE.