We have molecularly cloned the provirus of the avian musculoaponeurotic fibrosarcoma virus AS42.

The protective effect of a mouse hepatitis virus type-4 (MHV-4)-specific CD8+ cytotoxic T cell clone and a CD4+ helper T cell clone was examined by the adoptive transfer into brains of mice lethally infected with MHV-4. Mice survived acute encephalitis if more than 5 x 10(5) cells of either type of the virus-specific T cell clones had been transferred into H-2-matched recipients by 1 day post-infection. Although the adoptive transfer of both types of the T cell clones suppressed viral growth and viral antigen-positive cells in the brains, a significant inhibition of virus replication by the cytotoxic T cell clone was detected prior to that induced by the helper T cell clone. Histologically, cell destruction was prominent in the brains of mice which received the cytotoxic T cell clone. These results demonstrate that both the CD8+ cytotoxic T cell and the CD4+ helper T cell can protect mice from a lethal MHV-4 infection in the central nervous system.

Senile plaques (SPs) and cerebral amyloid angiopathy (CAA), pathological hallmarks of Alzheimer's disease, have not been thoroughly investigated histopathologically in nonhuman primates. To determine the onset age and histopathological characteristics of SPs and CAA, we examined the brains of 64 cynomolgus monkeys (Macaca fascicularis) from 2 to 35 years old. Mature (classical and primitive) plaques appeared in 16 out of 25 monkeys that were >20 years old. Moreover, mature plaques were observed more frequently than diffuse plaques and were located in the temporal cortex of the superior or inferior gyri and amygdala. Diffuse plaques in contrast to mature plaques did not show definite tendencies in onset age and distribution. CAA appeared in more than 22-year-old monkeys in 10 out of 16 animals and was frequently observed in capillaries and often found adjoining mature plaques. During immunohistochemical examination, an antiserum for amyloid beta protein (A beta) 1-40 could detect all SPs, whereas a monoclonal antibody for A beta 8-17 could not detect any diffuse plaques and only one third of the primitive plaques. As for CAA, the polyclonal antiserum was more sensitive than the monoclonal antibody. The present study describes the histopathological features of SPs and CAA in old cynomolgus monkeys.

Senile plaques were found in the cerebral cortices of three very aged cats (more than 18 years old). The plaques consisted of a coarse assembly of silver staining-positive materials, and was morphologically different from the well-known classical, primitive, and diffuse plaques. Congophilic amyloid angiopathy was observed in a few cortical arterioles of the oldest cat (20 years old). The senile plaques and a few cortical blood vessels were immunopositive for amyloid beta-protein (A beta). A beta-positive materials were also sparsely distributed in the cortical neuropil but did not form senile plaques there. These findings should help to clarify the development of senile plaques and the early stage of A beta deposition.

No abstract

Senile plaques (SPs) were found in the cerebral cortex of a 44-year-old Western lowland gorilla (Gorilla gorilla gorilla). All the SPs were obtained as dense assemblies consisting of fibrous materials by silver impregnation, but were not detected by Congo red. More SPs were detected by immunostaining for amyloidβ protein (Aβ) and a half of Aβ-positive-SPs were also immunoreactive for apolipoprotein E. Moreover, all SPs were immunoreactive for Aβ 42 and Aβ 43, but not for Aβ 40. SPs also did not contain Aβ precursor protein-positive structures. These findings suggested that SPs in this case were diffuse plaques. To our knowledge, this is the first report of SPs in the gorilla.

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Amyloid angiopathy with cerebral hemorrhage and senile plaques was found in the brain of aged dogs. In all 9 cases examined, 13 to 19 years old, 6 males and 3 females, amyloid deposits were observed mostly in the wall of cerebral arterioles and capillaries showed hyaline degeneration. The accumulation of amyloid fibrils measuring about 10 nm in diameter was seen in the cerebral vessel wall by electron microscopy. The cerebral hemorrhage was observed in 6 of 9 dogs and 2 of them showed massive hemorrhage. The hemorrhagic foci were sometimes closely contact with the vessels involved in amyloid angiopathy. In addition, senile plaques being classified into 2 types were found in the cerebral cortex of 3 dogs. The first type was characterized by the accumulation of degenerative neurites and often contained granular argyrophilic material. The second type had a well-defined amyloid core with neuritic halo. Amyloid deposits were also found in or around intestinal vessel walls of 3 dogs. The amyloid deposited in the cerebral vessels, senile plaques and intestinal vessels showed characteristic green birefringence under the polarized light even after potassium permanganate treatment.