Outbreaks of an acute febrile disease of cattle occurred in Japan in 1959 and 1960. Its occurrence was limited in late summer and autumn, and in Kyushu, Shikoku and Honshu roughly south of 37 degrees north latitude, suggesting a close correlation of the incidence with the climatic conditions, hence a possibility of the presence of arthropod vector. The disease was characterized by fever and lesions affecting the mucous membrane and skin, musculature and vascular system. Degeneration of striated muscles was observed in the esophagus, larynx, pharynx, tongue and skeletal muscular system. Edema and hemorrhage were marked in the mouth, lips, abomasum, coronets etc., occasionally followed by degeneration of the epithelium leaving erosions or ulcerations. Severe lesions affecting the esophageal and laryngopharyngeal musculature caused deglutitive difficulty which in turn resulted in dehydration and emaciation, and occasionally in aspiration pneumonia, constituting the major causes of death of the affected animals. These findings indicate that the disease resembles bluetongue in sheep and cattle. The clinical materials obtained from natural cases induced a clinical illness when inoculated into calves, and the disease was transmitted serially in calves by intravenous inoculation of the blood obtained at the height of febrile reaction. The experimentally produced disease was clinically and pathologically indistinguishable from the natural disease.

Previous serolgoical studies strongly suggested Akabane virus to be the etiologic agent of epizootic abortion and congenital arthrogryposis-hydranencephaly in cattle, and this view was further corroborated in this study by the isolation of the virus from an aborted fetus in an epizootic of the disease and from a fetus extracted froma cow which was suggested by serologic tests to have a recent infection with the virus. The latter fetus had histological changes of encephalomyelitis and polymyositis, and specific antigens of Akabane virus was shown by the immunofluorescent technique in brain tissues as well as skeletal muscular tissues. The virus was recovered from various fetal tissues and fluids, and in relatively large amounts from brain, spinal cord, cerebral fluid, skeletal muscles and fetal placenta. The intracranial inoculation of suckling mice, 1-2 days of age, was the most sensitive system for Akabane virus isolation and HmLu-1, a continuous cell line from hamster lung, seemed almost as sensitive as suckling mice.

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Sato, K., Inaba, Y., Kurogi, H., Takahashi, E., Satoda, K., Omori, T. and Matumoto, M.t 1977. Hemagglutination by calf diarrhea coronavirus. Vet. Microbiol., 2: 83--87.The virus was grown in BEK-1 cells, a stable cell line from bovine embryo kidney, and tested for hemagglutinafion (HA) with erythrocytes of a variety of species at 4°C, room temperature and 37°C. HA was observed at all temperatures with chicken, mouse, rat, and hamste~ erythrocytes but not with erythrocytes of human (O), cattle, horses, ~heep, guinea pigs, geese, duck~, pigeons and l-day-old chicks. Chickens showed a~ individual variation in agglutinability of their erythrocytes, requiring selection of birds to obtain erythrocytes for HA. HA reaction was inhibited by specific antiserum. Some factors involved in HA and HA inhibition (HI) were investigated and standard HA and HI tests were worked out.

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Entry of Epstein‐Barr virus into human lymphoblastoid cells (Daudi cells) was studied by electron microscopy. At the site of viral attachment, two distinct interactions conducive to penetration of the virus occurred between the viral envelope and cell membrane, namely, (i) simultaneous dissolution of both the envelope and cell membrane, presumably resulting in passage of viral capsids into the cytoplasm and (ii) dissolution confined to the cell membrane with resulting penetration of enveloped virus. In the latter case envelope dissolution appears to occur subsequently in the cytoplasm with release of capsids. Fusion of the viral envelope with the cell membrane was not observed. The capsids exhibited two distinct structural forms—one dense, the other translucent or light in appearance. The former disrupted near the cell membrane with release of viral cores into the cytoplasm whereas the light capsids containing dense cores migrated toward the nucleus and accumulated in the perinuclear region. Apparently the process of releasing deoxyribonucleic acid (DNA) from the light capsid is slowed down or prevented in Daudi cells. A hypothesis is presented concerning the manner in which these two types of capsids initiate infection.

SummaryAn inactivated vaccine prepared from virus grown in hamster hmg cells produced specific neutralizing antibody by intramuscular inoculation in cattle as well as in mice. Antibody response of cattle after one dose of vaccine was poor both in antibody level and seroconversion rate. However, a second dose given at intervals of 3 or more weeks induced a rapid and high-titered antibody formation in almost all animals. The antibody levels thus attained declined rather rapidly in several months, yet a booster dose given one year later provoked a rapid antibody response. Considering this pattern of antibody response together with the seasonal incidence of the disease it seems adequate that the initial immunization with two doses and the booster inoculation be made in late spring or early summer, immediately before the epizootic season. The vaccination prevented the disease in calves challenged with virulent virus. The vaccine exerted little side effects in cattle. Cows vaccinated during pregnancy gave birth to healthy calves in term. No adverse effects of vaccination on milk prodnetion was shown. All these findings indicate efficacy and safety of the vaccine, although the final evaluation rests on largescale field trials.