Isolation of Aino virus from an aborted bovine fetus.

A male fetus of gestation day 187 was aborted from a Holstein-Friesian cow in an epizootic of the Aino virus (AINOV) in September 1995. Neutralizing antibody titers against AINOV were 1:128, 1:16 and 1:64 in the dam serum, fetal ascites and cerebrospinal fluid, respectively. A 10% brain suspension of the aborted fetus was prepared immediately after autopsy, rinsed three times and sonicated before centrifugation. The supernatant was then inoculated into HmLu-1 cell cultures. A cytopathic effect was noted on post-inoculation day 7. The isolated virus was identified as the AINOV based on the physicochemical properties and cross neutralization test. This is the first report on the isolation of AINOV from an aborted bovine fetus.

Aino virus antigen in brain lesions of a naturally aborted bovine fetus.

A bovine fetus aborted at 187 days of gestation was serologically and immunohistopathologically examined. Serum and cerebrospinal fluid samples had high titers of virus-neutralizing antibody for Aino virus. A severe necrotizing encephalopathy was noted. Aino virus antigen was demonstrated in neuroglial cells within the brain lesion. The destruction of developing neuronal cells appeared to be a significant feature of the pathogenesis of lesions due to Aino virus infection in the central nervous system.

Immunohistochemical expression of microtubule-associated protein 5 (MAP5) in glial cells in multiple system atrophy.

An immunohistochemical study focusing on glial cells was performed using monoclonal antibodies against microtubule-associated proteins (MAP1, MAP2 and MAP5), transferrin, leukocyte common antigen (LCA) and glial fibrillary acidic protein (GFAP) in 5 cases of multiple system atrophy (MSA) exhibiting olivopontocerebellar atrophy and striatonigral degeneration. An antibody to MAP5, a fetal antigen in developing brain, was strongly demonstrated in the glial cytoplasmic inclusions (GCIs) which have recently drawn a great deal of attention and were observed in all 5 cases of MSA. Moreover, MAP5-positive glial cells (MAP5-Gs) were present in significantly higher number than in the controls in various regions where GCIs were found, predominantly in putamen, substantia nigra, cerebellar white matter and internal capsule. LCA and transferrin, markers of microglia and oligodendroglia, respectively, were immunohistochemically detected in some MAP5-Gs. GFAP, on the other hand, was not expressed in MAP5-Gs at all. These findings suggest that MAP5-Gs consist of reactive microglia and oligodendroglia. Our study is the first to demonstrate immunohistochemical detection of MAP5 in glial pathological changes in MSA.

Abnormal molecules of mitochondrial aspartate aminotransferase in the liver of vitamin B-6--deficient rats may be produced in the mitochondrial matrix.

The distribution of mitochondrial aspartate aminotransferase (AspATm) in liver cells was studied in rats fed pyridoxine-deficient and control diets. Mitochondrial aminotransferase activity was found mainly in the matrix fraction, with smaller amounts in the outer membranes, intermembrane space and cytosol. The precursor of the enzyme was detected in the liver cytosol of both vitamin B-6--deficient and control rats, and its amount was similar in the two groups. When pyridoxal phosphate was added to the assay system, the ratio of enzyme activity to antigenic activity (E/A) of mitochondrial aspartate aminotransferase in the cytosol of both vitamin B-6--deficient and control rats was about 70% of that in the matrix of control rats. On the other hand, the E/A of the matrix enzyme in deficient rats was 53% of that of controls. From these results we concluded that pyridoxal phosphate is not necessary for translocation of mitochondrial aspartate aminotransferase into mitochondrial matrix and that abnormal molecules of the enzyme may be formed in the matrix of vitamin B-6--deficient rat liver.