Studies with rinderpest virus in tissue culture

Plowright, W.; Ferris, R.D.

doi:10.1007/bf01241304

Cited by 48 publications

(8 citation statements)

References 14 publications

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“…The technique employed was that described by Plowright & Ferris (1961) and all sera were tested against a 10-2 dilution of the same virus stock, providing a mean of 1024 TCD50 per tube. RESULTS Table 1 gives some details for twenty-three cattle which were killed or died after the onset of fever.…”

Section: Evaluation Of the Resultsmentioning

confidence: 99%

“…All of them were approximately 2 years old and twenty-two of them had, apparently, a large proportion of the blood of the highly susceptible Channel Islands breeds (Guernsey and Jersey). Their sera were found to be negative in screening tests for rinderpest-neutralizing antibody (Plowright & Ferris, 1961) and they were housed in isolation units which precluded the possibility of accidental infection. They were fed with hay only and provided with water ad lib.…”

Section: Methodsmentioning

confidence: 99%

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Studies on the pathogenesis of rinderpest in experimental cattle II. Proliferation of the virus in different tissues following intranasal infection

Plowright

1964

J. Hyg.

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The pathogenesis of rinderpest virus was studied in twenty-nine grade cattle, which were infected by the intranasal route with a virulent strain of virus recently isolated in East Africa (RGK/1). These animals were killed or died at intervals of 1–16 days after infection and a number of tissues from each of them (usually 21) was titrated for virus infectivity in monolayer cultures of primary bovine kidney cells.Temperature reactions were first detected on the 3rd to 5th days (mean 4·1), mouth lesions on the 6th to 9th and diarrhoea on the 8th or 9th days, following infection. The course of the disease was divided into four phases, viz. incubation (days 1–4), prodromal (days 5–7), mucosal (days 8–12) and early convalescence (days 13–16). Virus proliferation in different tissues was related to these clinical phases, detailed results being presented in tabular and graphical form.No primary multiplication was detected in the nasal mucosa but virus was demonstrable within 48 hr. in its associated lymph nodes. Low-level viraemia began on the 2nd or 3rd days after infection and generalization had occurred by the end of the incubation period. The virus had established itself at this time throughout the alimentary tract and, sometimes, in the lungs.The prodromal phase was characterized by plateaux of high virus titres in the lymphopoietic and lympho-epithelial tissues; there was a descending gradient from the cephalic nodes to the superficial lymph and haemolymph nodes of the body, to the visceral lymph nodes and spleen. There was a similar gradient in the titre of virus in the mucosae of the gastro-intestinal tract—from caecum to colon, to ileum and pylorus. Virus first appeared in the turbinate mucosa on the 5th day, post-infection and lung titres were high towards the end of this period. Some virus proliferation may have occurred in the liver, but none was certainly demonstrable in the kidney, myocardium or brain.The mucosal phase began with continuing high titres of virus in all the major sites of proliferation, but a decline set in from the 9th day onwards. This at first involved the cephalic lymph nodes but soon extended to the spleen and other lymphopoietic tissues. It was most delayed in lympho-epithelial structures such as the tonsil, lung and gastro-intestinal mucosae. It was suggested that the decline in virus titres was due to the destruction of susceptible cells, accompanied by the local production and later circulation of antibody. Neutralizing antibody was present in the serum on and after the 9th day.During the early convalescent period virus had disappeared from four animals, with the exception of one recovery from the lung tissue. Antibody titres were high during this time.These results were discussed with reference to previously existing information on the distribution of rinderpest virus in infected cattle. An attempt was made to correlate them with published information on the pathogenesis of human measles and canine distemper. The data were also used to explain some previously reported observations on the excretion of rinderpest virus by experimentally infected cattle.This study would not have been possible without the enthusiastic co-operation of Messrs C. S. Rampton, A.I.M.L.T., R. F. Staple, A.I.M.L.T., and R. Pillinger, F.I.M.L.T., in organizing and carrying out a very considerable number of laborious titrations. Dr B. Liess helped with some of the animals killed at earlier stages of the infection. Our junior African staff gave invaluable assistance with their careful and efficient handling of many thousands of tissue cultures; amongst them we should particularly like to mention Mr Francis Ngugi and Mr Harrison Agili.This paper is published with the permission of the Director, E.A.V.R.O., Mr H. R. Binns, C.M.G., O.B.E.

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Section: Evaluation Of the Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Studies on the pathogenesis of rinderpest in experimental cattle II. Proliferation of the virus in different tissues following intranasal infection

Plowright

1964

J. Hyg.

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“…von Ostertag and Bugge (1906) observed clinical relapses over a period of several months in some animals, and Plowright and Ferris (1959a) observed (in cattle which were recovering from infection with a mild strain of rinderpest virus) a recurrence of papular stomatitis. Schaaf et a1 ( 1940) did not observc any relapses after the healing of papules, and were of the opinion that infection Droduced a high degree of immunity which possibly lasted at least 5 months.…”

Section: Shows Ballooning Degenerat I O N Of Epithelial Cells S H mentioning

confidence: 95%

A PAPUL.4R Stomatitis of Virus Origin in Australian Cattle

Snowdon

French

1961

Aust Veterinary J

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“…The DNA sequences were determined on both strain (RPV-K) [1], the vaccine (RBOK) strain (RPV-R) [1], the Edmonston strain of MV [5] and the Yanaka strain of CDV [submitted data]. The RPV-R strain was originally derived from the RPV-K strain by repeated passages in primary bovine kidney cells [15]. The entire nucleotide sequence of the M gene of RPV-L had the same number of nucleotides as the RPV-K and RPV-R.…”

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confidence: 99%

Molecular Properties of the Matrixprotein(M) Gene of the Lapinized Rinderpest Virus.

Shiotani

Miura

Fujita

et al. 2001

The Journal of Veterinary Medical Science

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ABSTRACT. The nucleotide sequence of the matrixprotein (M) gene of the lapinized rinderpest virus (RPV-L) was determined. The fulllength cDNA of the RPV-L M gene is composed of 1460 base pairs and is supposed to contain an open reading frame of 1005 nucleotides encoding on M protein of 335 amino acids. The homology of the predicted amino acid among congeneric morbilliviruses such as RPV Kabete 'O' strain (wild strain of RPV), RPV RBOK strain (vaccine strain of RPV for cattle), measles virus (MV), and canine distemper virus (CDV), is approximately 94%, 93%, 87% and 77%, respectively. In the present study, all coding regions of the RPV-L strain have been determined. KEY WORDS: lapinized strain, M gene, rinderpest virus.

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Studies with rinderpest virus in tissue culture

Cited by 48 publications

References 14 publications

Studies on the pathogenesis of rinderpest in experimental cattle II. Proliferation of the virus in different tissues following intranasal infection

Studies on the pathogenesis of rinderpest in experimental cattle II. Proliferation of the virus in different tissues following intranasal infection

A PAPUL.4R Stomatitis of Virus Origin in Australian Cattle

Molecular Properties of the Matrixprotein(M) Gene of the Lapinized Rinderpest Virus.

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