Nucleotide sequence of capsid protein gene of porcine parvovirus.

Approximately 90% of the genome of porcine parvovirus was cloned into bacterial cells. The nucleotide sequence of the genome from 33 map units (MU) to 95 MU was determined and shown to include the entire gene encoding the capsid proteins. The predicted amino acid sequences of the capsid proteins showed extensive homology to those of other autonomous parvoviruses.

Cooperative regulation of bovine leukaemia virus gene expression by two overlapping open reading frames in the XBL region.

Bovine leukaemia virus (BLV) induces syncytia in productively infected ovine and bovine monolayer cells. Expression of the env gene directly determines the syncytium-forming activity, since the expression of a cloned env gene directed by the simian virus 40 (SV40) early promoter efficiently induced syncytia in transfected ovine embryonic (OE) cells. However a BLV long terminal repeat (LTR)-directed expression plasmid (pLTRenv) failed to induce syncytia in transfected OE cells, suggesting insufficient promoter activity of the LTR sequences. To assess the role of the XBL genes, which are located in the 3' distal region of the genome, in viral gene expression we constructed SV40 early promoter-directed expression plasmids. These contained open reading frames (ORFs) in the XBL region, and were examined for syncytium-inducing activity by cotransfection with pLTRenv. The results suggest that both XBL-I (the longest ORF: x-lor) and XBL-II (a shorter overlapping ORF: x-sor) are trans-acting genes which cooperatively activate LTR-directed viral gene expression.

Clinico-biochemical studies on fattening cattle with stiff gait as main symptom in Japan.

The chemical compositions of blood and bone were estimated in eight affected cattle as part of clinico-biochemical studies on a disease of beef cattle for fattening with stiff gait of the four limbs, strange posture, and elongation and deformation of the hoofs as main symptoms. Eight of the affected cattle were divided into two groups from the results of some examinations. Radiographical changes, such as the deformation, atrophy and lack of the apex of the third phalanx, were remarkable in five affected cattle (Nos. 1, 2, 4, 5 and 6; group A), but not so remarkable in three (Nos. 7, 8 and 9: group B). The blood composition was within a normal range in group A. On the other hand, total serum protein, urea nitrogen, calcium and inorganic phosphorus were a little lower and magnesium and potassium higher in blood level in group B than in control cattle. The pH of rumen juice was within a range of 6.0 to 6.5 in all the effected cattle. The differences of components of phalanges were remarkable between the two groups. Namely, in group A, the magnesium and sodium levels of phalanges were higher than in control cattle. Ash and calcium contents increased distinctly at the tip of the third phalanges were higher than in control cattle. On the other hand, in group B, ash, calcium, sodium and potassium contents were lower than in control cattle. The fat content was much higher in the affected groups than in the control group. There wer slight changes in the inorganic component levels of the ungual layer. These changes were proportional to those of the phalanges.

Equine infectious anemia virus from infected horse serum.

Equine infectious anemia virus was purified from infected horse serum samples. Electron microscope observation on negatively stained preparations of purified virus showed roughly spherical particles sized between 100 and 200 nm in diameter. In disrupted particles, an envelope was visible but no internal structure could be resolved. Since the purified virus fraction had a strong antigenic activity to antiserum in immunodiffusion reaction, these particles are thought to be the causative virus of equine infectious anemia.

Study of the one-step growth curve of equine infectious anemia virus by immunofluorescence.

Primary horse leukocyte cultures were inoculated with 2 or 10 50% tissue culture infective doses (TCID(50)) of equine infectious anemia (EIA) virus per cell, and the titer of cell-associated and fluid-phase virus was determined from 1 to 72 hr postinoculation (PI). Cover slips were collected from 4 to 72 hr PI and stained for EIA viral antigen by the indirect immunofluorescent (FA) technique. Viral replication was detected after a latent period of approximately 18 to 24 hr and reached peak titers of approximately 10(4.5) to 10(6) TCID(50)/0.5 ml from 48 to 72 hr PI. The fluid phase contained 10(1) to 10(2) TCID(50)/0.5 ml more virus than the cells. Viral antigen was first detected by FA from 18 to 24 hr PI. Approximately 75% of the cells contained antigen in their cytoplasm 72 hr PI. The FA technique is a sensitive method for detecting EIA virus in horse leukocyte cultures.

Immunodiffusion studies of purified equine infectious anemia virus.

Antigenicity of purified equine infectious anemia (EIA) virus was examined by immunodiffusion against sera obtained from horses experimentally infected with EIA virus. The purified virus reacted with the infected horse serum, and virus-specific precipitating antibody was demonstrated. Furthermore, it was found that purified EIA virus reacted against the serum of horses infected with all strains of EIA virus which were antigenically different from one another. From the result, group-specific components of the virus rather than strain-specific ones were considered to be involved in the reaction. Serological reactivity was lost by adding antiserum from the infected horse to the antigen. The precipitating antibody usually appeared in the serum 1 to 2 weeks after the first febrile attack of EIA and remained for a longer period. Some characteristics of the purified antigen and specificity of the reaction for EIA are described.