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Influenza in western australia 1968 to 1969
ABSTRACTS OF ANNUAL SCIENTIFIC MEETING
1970
59
THE BEHAVIOUR OF MURINE SARCOMA (VIRUS-INDUCED) TUMOUR CELLS IN VITRO
SIMONS, P. J. Department of Microbiology, University of Western Australia, Perth, Western Australia In 1964, D r J. Harvey of the London Hospital isolated an unusual variant virus from one strain of murine leukaemia virus. Unlike the original leukaemia virus the variant is able to induce solid twnours at the site of inoculation and consequently has been called murine sarcoma virus (MSV). MSV inoculated intramuscularly into newborn Prince Henry mice induces a tumour which morphologically appears to be a haemangiosarcoma. Cells from MSV-induced tumours can be established in tissue culture. Early passages of such cultures have an unusual appearance with clumps of densely staining spindle cells separated by large multinucleate cells. Clones of cells were isolated from these cultures using collagen-coated petri dishes. Six clones were grown up to mass culture. All 6 cell clones continuously released MSV in the culture medium. As the cell monolayers grew to confluence there was fusion of cells, with the appearance of myotube-like structures. The changes took place only when the cells were grown in collagen-treated dishes. Using regular tissue culture plastic petri dishes, the cells grew poorly in the form of clumps. INFLUENZA IN WESTERN AUSTRALIA 1968 TO 1969
MACKAY-SCOLLAY, E., HOBDAY, JOY 19HARNETT, G. Department of Public Health, Perth, Western Australia A report was given on the laboratory investigation of outbreaks of respiratory virus infections in Western Australia during the winters of 1968 and 1969. Influenza virus B was associated with the outbreak of 1968, whereas influenza A (A,/Hong Kong/1968) was the cause of the widespread epidemic of 1969. Epidemiological aspects of the 2 epidemics were discussed, particularly: (a) the failure of influenza virus A,/Tokyo/1967, although the virus was isolated from the throats of naval recruits arriving from the Eastern States, to cstab!ish infection in the personnel of the naval training base as a whole before the epidemic broke out; (b) the failure of influenza virus A,/Hong Kong/1968 to cause clinical influenza in the months intervening between the winters of 1968 and 1969 despite the sporadic isolation of the virus; (c) the influence of weather and of vaccination on the timing and extent of the epidemic. A STUDY OF THE FORM OF EXPERIMENTAL CLEFT PALATE IN RATS
LOVE, ALDYTH M. University of Queensland, Brisbane, Queensland It is generally accepted that cleft palate results from a complex interaction of genetic and environmental factors. In consequence, the findings of different experimental workers are difficult to compare. To simplify background influences, cleft palate was produced in a closed colony of Sprague-Dawley rats with vitamin A, 6-mercaptopuMe, meclozine and amniocentesis. Each technique yielded lesions which, on study, showed a number of characteristic features. Hypervitaminosis A induced total and incomplete clefts, the latter involving hard and soft palate. Prognathia and micrognathia could occur, and there were often basocranial defects with deformity of the pharynx and Eustachian tubes. With 6-mercaptopurine, total and incomplete clefts were seen, but when only the soft palate was affected, the cleft was often asymmetrical. Very severe micrognathia but not prognathia could exist, and fusion of touching oral surfaces was minimal. Meclozine always produced total clefts with variable micrognathia, and fusion of touching oral surfaces was usual. Amniocentesis evoked total and incomplete clefts, the latter usually anteriorly placed. Among the conclusions which might be drawn, the following have general interest. 1. Delayed normal development does not adequately explain the variety of the clefts and their associated lesions, with the corollary that maldevelopment rather than retarded development underlies at least some of these anomalies. 2. As an extension of the above, cleft palate formation can result from multiple mechanisms. 3. Because clefts produced by amniocentesis were different from those following chemical teratogens, it is unlikely that disturbed amniotic fluid dynamics (especially oligohydramnios) played an important pan in cleft production by the latter.
1970
59
THE BEHAVIOUR OF MURINE SARCOMA (VIRUS-INDUCED) TUMOUR CELLS IN VITRO
SIMONS, P. J. Department of Microbiology, University of Western Australia, Perth, Western Australia In 1964, D r J. Harvey of the London Hospital isolated an unusual variant virus from one strain of murine leukaemia virus. Unlike the original leukaemia virus the variant is able to induce solid twnours at the site of inoculation and consequently has been called murine sarcoma virus (MSV). MSV inoculated intramuscularly into newborn Prince Henry mice induces a tumour which morphologically appears to be a haemangiosarcoma. Cells from MSV-induced tumours can be established in tissue culture. Early passages of such cultures have an unusual appearance with clumps of densely staining spindle cells separated by large multinucleate cells. Clones of cells were isolated from these cultures using collagen-coated petri dishes. Six clones were grown up to mass culture. All 6 cell clones continuously released MSV in the culture medium. As the cell monolayers grew to confluence there was fusion of cells, with the appearance of myotube-like structures. The changes took place only when the cells were grown in collagen-treated dishes. Using regular tissue culture plastic petri dishes, the cells grew poorly in the form of clumps. INFLUENZA IN WESTERN AUSTRALIA 1968 TO 1969
MACKAY-SCOLLAY, E., HOBDAY, JOY 19HARNETT, G. Department of Public Health, Perth, Western Australia A report was given on the laboratory investigation of outbreaks of respiratory virus infections in Western Australia during the winters of 1968 and 1969. Influenza virus B was associated with the outbreak of 1968, whereas influenza A (A,/Hong Kong/1968) was the cause of the widespread epidemic of 1969. Epidemiological aspects of the 2 epidemics were discussed, particularly: (a) the failure of influenza virus A,/Tokyo/1967, although the virus was isolated from the throats of naval recruits arriving from the Eastern States, to cstab!ish infection in the personnel of the naval training base as a whole before the epidemic broke out; (b) the failure of influenza virus A,/Hong Kong/1968 to cause clinical influenza in the months intervening between the winters of 1968 and 1969 despite the sporadic isolation of the virus; (c) the influence of weather and of vaccination on the timing and extent of the epidemic. A STUDY OF THE FORM OF EXPERIMENTAL CLEFT PALATE IN RATS
LOVE, ALDYTH M. University of Queensland, Brisbane, Queensland It is generally accepted that cleft palate results from a complex interaction of genetic and environmental factors. In consequence, the findings of different experimental workers are difficult to compare. To simplify background influences, cleft palate was produced in a closed colony of Sprague-Dawley rats with vitamin A, 6-mercaptopuMe, meclozine and amniocentesis. Each technique yielded lesions which, on study, showed a number of characteristic features. Hypervitaminosis A induced total and incomplete clefts, the latter involving hard and soft palate. Prognathia and micrognathia could occur, and there were often basocranial defects with deformity of the pharynx and Eustachian tubes. With 6-mercaptopurine, total and incomplete clefts were seen, but when only the soft palate was affected, the cleft was often asymmetrical. Very severe micrognathia but not prognathia could exist, and fusion of touching oral surfaces was minimal. Meclozine always produced total clefts with variable micrognathia, and fusion of touching oral surfaces was usual. Amniocentesis evoked total and incomplete clefts, the latter usually anteriorly placed. Among the conclusions which might be drawn, the following have general interest. 1. Delayed normal development does not adequately explain the variety of the clefts and their associated lesions, with the corollary that maldevelopment rather than retarded development underlies at least some of these anomalies. 2. As an extension of the above, cleft palate formation can result from multiple mechanisms. 3. Because clefts produced by amniocentesis were different from those following chemical teratogens, it is unlikely that disturbed amniotic fluid dynamics (especially oligohydramnios) played an important pan in cleft production by the latter.