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Biomedical subjects

J Hotchin

Publications and source records attributed to J Hotchin.

At least 37 records · Page 2Linked to original sources

Role of substrains in persistent lymphocytic choriomeningitis virus infection.

Two plaque-type mutants, a wild strain MB(1), and a slow-growing non-plaque-forming variant of LCM virus were compared in L cell cultures. The cultures were monitored at biweekly intervals following infection for plaque-forming virus titre and cytoplasmic and membrane specific immunofluorescence of the cells. Different patterns were obtained in each case and the relevance of these results to LCM persistence is discussed. While the LM variant continually produced virus for 35 transfers, with a cycling titre, the SC variant stopped producing detectable virus after 30 transfers. Thereafter this culture remained fluorescent and resembled the one infected with the slow-growing variant. The degree of specific immunofluorescence of both continued to cycle. The MB(1) strain stopped producing virus after the 18th transfer.

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Laboratory diagnosis of lymphocytic choriomeningitis.

Current laboratory methods for the diagnosis of lymphocytic choriomeningitis are discussed, mainly from the point of view of recent improvements. The use of sentinel guinea-pigs is suggested for the detection of lymphocytic choriomeningitis infection in animal colonies.

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Lymphocytic choriomeningitis in a hamster colony causes infection of hospital personnel.

A series of febrile illnesses, some severe, among hospital personnel was traced to an outbreak of lymphocytic choriomeningitis in a hospital research colony of Syrian hamsters. By rapid virus isolation and identification techniques, a definitive diagnosis was made 5 days after specimens were received. This outbreak emphasizes the dangers of working with experimental hamsters and tumor cell lines passaged in them.

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Lytic and turbid plaque-type mutants of lymphocytic choriomeningitis virus as a cause of neurological disease or persistent infection.

Mouse-passaged lymphocytic choriomeningitis (LCM) virus was found to contain a mixture of two different plaque-type mutants when plated on BHK-21/13S cells in agarose suspension. One mutant gave rise to clear plaques, with death of the cells, whereas the other produced turbid plaques which were sometimes very difficult to see. The clear-plaque variant caused a pronounced cytopathic effect on BHK-21 cells, but the turbid variant caused none; it also interfered with the cytopathic effect due to the clear variant. Brain-passed LCM virus was found to consist mainly of the clear-plaque-type, whereas liver-passed virus was mainly turbid-plaque-type. The clear type induced convulsions and early death after intracerebral inoculation of adult mice; the turbid variant caused no convulsions and late deaths. In newborn mice, the clear-plaque-type was uniformly fatal, whereas the turbid variant caused no deaths but instead induced persistent tolerant infection.

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Thymus-dependent lymphocytes: destruction by lymphocytic choriomeningitis virus.

Selective destruction of small lymphocytes in the thymusdependent areas of lymph nodes and thymocytes was observed in mice infected with lymphocytic choriomeningitis virus. These changes were clearly evident in lymphoid and splenic tissue 3 days after infection and in the thymus by day 7. The destructive changes paralleled growth of the virus in these organs. The findings show that infection with lymphocytic choriomeningitis virus can temporarily cause the equivalent effect of neonatal thymectomy, that is, a "viral thymectomy," which appears to be related to the ability of this virus to cause persistent infection.

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