The P/C mRNA of Sendai virus (SeV) encodes a nested set of accessory proteins, C, C, Y1, and Y2, referred to collectively as C proteins, using the ؉1 frame relative to the open reading frame of phospho (P) protein and initiation codons at different positions. The C proteins appear to be basically nonstructural proteins as they are found abundantly in infected cells but greatly underrepresented in the virions. We previously created a 4C(؊) SeV, which expresses none of the four C proteins, and concluded that the C proteins are categorically nonessential gene products but greatly contribute to viral full replication and infectivity (A. Kurotani et al., Genes Cells 3:111-124, 1998). Here, we further characterized the 4C(؊) virus multiplication in cultured cells. The viral protein and mRNA synthesis was enhanced with the mutant virus relative to the parental wild-type (WT) SeV. However, the viral yields were greatly reduced. In addition, the 4C(؊) virions appeared to be highly anomalous in size, shape, and sedimentation profile in a sucrose gradient and exhibited the ratios of infectivity to hemagglutination units significantly lower than those of the WT. In the WT infected cells, C proteins appeared to colocalize almost perfectly with the matrix (M) proteins, pretty well with an external envelope glycoprotein (hemagglutinin-neuraminidase [HN]), and very poorly with the internal P protein. In the absence of C proteins, there was a significant delay of the incorporation of M protein and both of the envelope proteins, HN and fusion (F) proteins, into progeny virions. These results strongly suggest that the accessory and basically nonstructural C proteins are critically required in the SeV assembly process. This role of C proteins was further found to be independent of their recently discovered function to counteract the antiviral action of interferon-␣/␤. SeV C proteins thus appear to be quite versatile.Sendai virus (SeV) is an enveloped virus with a linear, nonsegmented, negative-sense RNA genome of 15,384 nucleotides. It belongs to the genus Respirovirus of the family Paramyxoviridae. The genome encodes, in a 3Ј-to-5Ј order, the nucleocapsid (N) protein, phospho (P) protein, matrix (M) protein, fusion (F) protein, hemagglutinin-neuraminidase (HN), and large (L) protein. The genome RNA is tightly encapsidated with the N protein subunits and is further complexed to the polymerase comprising the L and P protein subunits (14). This ribonucleoprotein (RNP) complex represents the internal core structure of the virion. The viral envelope contains two glycoproteins, HN and F. The former mediates viral attachment to the surface of susceptible cells, and the latter is required for the fusion of the envelope with the cellular membrane to introduce the genomic material into the cytoplasm. The envelope lipid bilayer is derived from the host cell plasma membrane during the final step of assembly by budding. There is a layer of M proteins between the envelope and RNP (30). The M protein has been thought to play a critical role in a...

ABSTRACT. On March 22, 1998, a mature, male, hyposthenic Pacific striped dolphin (Lagenorhynchus obliquidens) was stranded at Aoshima Beach in Miyazaki prefecture, Japan. A necropsy performed 14 hr after death revealed mild diffuse congestion and edema of the leptomeninges and mild pulmonary atelectasis. Histopathologically, non-purulent inflammatory were observed throughout the cerebrum, thalamus, midbrain, pons, medulla oblongata, and spinal cord. Hematoxylin and eosin stain revealed no viral inclusion bodies. Immunohistochemistry using a monoclonal antibody against nucleoprotein of canine distemper virus (CDV-NP) revealed a number of CDV-NP-positive granular deposits in the cytoplasm and cell processes of the degenerating or intact neurons. The present paper is a first report of spontaneously occurred morbillivirus infection in a dolphin at the Pacific Ocean around Japan.-KEY WORDS: dolphin, encephalomyelitis, morbillivirus.

ABSTRACT. A gelatinous focus with cystic spaces, was found in the posterior funiculus of the 2nd to 3rd lumbar levels of the spinal cord of a Japanese Black heifer, 2 years old, with clinical signs of severe dysstasia. Histopathological examination revealed that the spinal lesion consisted of multifocal and diffuse proliferation of round cells with abundant vacuolar cytoplasm and hyperchromatic nuclei. In the lesions there was a number of cystic spaces containing aggregates of small round cells. The neoplastic foci showed a honeycomb structure divided by thin blood vessels, representing typical lesions of oligodendroglioma. Diffuse and multifocal proliferation of these round cells were also recognized in the subarachnoidal space in the sacral spinal cord. Immunohistochemically, the proliferating round cells were negative for glial fibrillary acidic protein. Based on these morphological features, the case was diagnosed as lumbar spinal oligodendroglioma with diffuse arachnoidal dissemination.-KEY WORDS: bovine, oligodendroglioma, spinal cord.J. Vet. Med. Sci. 61(12): 1323-1326, 1999 cord were also stained with Luxol fast blue (LFB), Masson's trichrome, Watanabe's silver impregnation, and alcian blue (pH 2.5). Histopathological examination revealed that the lumbar spinal lesion consisted of multifocal and diffuse proliferation of neoplastic cells with cystic spaces (Fig. 2). The tumor mass was located mainly in the white matter, and the posterior funiculus were almost totally replaced by the proliferating tumor cells and cystic places. The neoplastic foci showed a honeycomb structure with solid proliferation of round cells, representing the typical appearance of oligodendroglioma (Fig. 3). Most neoplastic cells were round in shape with abundant clear cytoplasm and hyperchromatic central nuclei. The presence of cytoplasmic processes was not confirmed. In the tumor there were a number of blood vessels with thin vascular walls, while the endothelial cells did not show apparent hyperplastic or proliferative changes. There were also a few of well differentiated astrocytes with well defined eosinophilic cytoplasmic processes in the neoplastic foci.In contrast, at the periphery of the neoplastic foci, diffuse proliferation of these astrocytes was prominent. Within the cystic spaces, there were aggregates of small number of small round cells mimicking lymphocytes, with small hyperchromatic round nuclei and scanty cytoplasm. Mitoses of the neoplastic cells were extremely rare. The neoplastic cells invaded the leptomeninges, and the subarachnoidal space was filled by a proliferation of these cells. Diffuse and multifocal proliferation of the round cells and lymphocyte-like small round cells, were also seen in the subarachnoidal space in the 2nd and 3rd levels of the sacral spinal cord (Fig. 4). In this area, some foci consisted of aggregates of neoplastic cells, and some areas showed an organoid structure made up of tumor cells, a few astrocytes and their cytoplasmic processes (Fig. 5). Besides the spinal cord there was no ...

ABSTRACT. Accumulating evidences indicate that an endotoxin originating from intestinal gram-negative bacteria may be involved in alcohol-induced liver injury including fatty liver. Therefore, whether immunization against intestinal bacterial endotoxin blocked fatty liver induced by chronic alcohol and diet including much-unsaturated fatty acid was investigated in rats. The titer of antibody against the endotoxin increased significantly after 13 weeks of continuous immunization. Daily alcohol treatment was initiated at 12 weeks and continued for 4 weeks. Plasma glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT) and triglyceride (TG) levels increased significantly in non-immunized rats receiving alcohol, but not in immunized rats. Continuous alcohol treatment gradually decreased the survival rate to 60% from 13 days after beginning administration in non-immunized, but not immunized, rats. A histochemical study revealed that continuous treatment with alcohol and unsaturated fatty acids caused fatty liver in non-immunized, but not immunized, rats. This study strongly supports the hypothesis that alcohol-induced fatty liver is due to a circulating endotoxin, and suggests that immunization for endotoxin prevent the alcoholic fatty liver.KEY WORDS: alcohol, endotoxin, fatty liver.