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Biomedical subjects

R E SHOPE

Publications and source records attributed to R E SHOPE.

At least 37 records · Page 2Linked to original sources
PubMed1959

Electron microscope study of the development of the papilloma virus in the skin of the rabbit.

Rabbit papilloma virus seems uniquely to begin its proliferation in the nucleolus of infected cells. In cells near the germinal layer of the stratum Malpighii spherical viral bodies seem to develop within a reticulum which forms out of the fine granular matrix of the nucleolus. The virus may later fill the nucleus and spread into the whole cell. The age of the cell, determined by its position in the Malpighian layer and by the extent of keratinization, can be correlated with the viral development.

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PubMed1958

An infectious cutaneous fibroma of the Virginia whitetailed deer (Odocoileus virginianus).

A naturally occurring cutaneous fibroma of deer has proven to be experimentally transmissible in deer. The causative agent is a virus that is readily alterable through Berkefeld N candles and that survives in fibroma tissue for at least as long as 27 months in glycerol-saline at -20 degrees C. The experimentally produced deer fibroma has an incubation period of about 7 weeks, a very slow rate of growth, and a high regression rate.

Animals↗
PubMed1958

The swine lungworm as a reservoir and intermediate host for hog cholera virus. II. Attempts to demonstrate the presence of hog cholera virus in lungworms derived from swine with cholera.

Suspensions of adult lungworms, procured from swine that were outwardly healthy but derived from eggs passed by swine with hog cholera, induced this disease in a small proportion of swine into which they were injected intramuscularly. This result was achieved in both lungworm-free and lungworm-infested swine, though perhaps slightly more regularly in the lungworm-infested animals. Swine that had had an intramuscular injection of lungworm suspension and that had remained normal, developed hog cholera much more regularly following the ingestion of lungworm larvae of cholera origin than did swine not previously injected with lungworms. The findings described were markedly dependent upon season and were regularly reproducible only during the first 4 or 5 months of the year. The results presented are considered as further evidence that the swine lungworm serves as reservoir and intermediate host for hog cholera virus and that the virus is ordinarily carried by the lungworm in a masked form which must be provoked to pathogenicity by some stress before it can cause obvious disease in swine.

Animals↗
PubMed1958

The swine lungworm as a reservoir and intermediate host for hog cholera virus. I. The provocation of masked hog cholera virus in lungworm-infested swine by ascaris larvae.

Evidence that the swine lungworm can serve as reservoir and intermediate host for the hog cholera virus has been presented. The virus, however, is ordinarily carried in a masked form and must be provoked to pathogenicity by some stress before it can cause apparent disease. In the present experiments, ascaris larvae supplied the provocation needed to induce hog cholera in swine carrying lungworms infected with masked hog cholera virus. Provocation of the masked virus by ascaris larvae was seasonal in that it was effective only during a period embracing the first 5 months of the year.

Animals↗
PubMed1957

The leech as a potential virus reservoir.

Leeches, fed on swine infected with hog cholera, contained virus for as long as 87 days after their infective blood meals. In three instances, infected leeches apparently transmitted hog cholera virus to susceptible swine in the process of normal feeding. Myxoma virus persisted in leeches for as long as 154 days after the ingestion of a blood meal from rabbits with myxomatosis. Leeches fed consecutively, first on swine with hog cholera, and later on rabbits with myxomatosis, acquired both viruses. In such dually infected leeches, the hog cholera virus persisted for as long as 122 days and the myxoma virus for as long as 110 days, the longest periods tested. Leeches fed consecutively, first on rabbits with myxomatosis, and later on swine with hog cholera, acquired only the myxoma virus. Hog cholera virus could not be demonstrated in such dually fed leeches. Myxoma and hog cholera viruses appeared to be present in about equivalent amounts in the anterior and posterior thirds of the bodies of infected leeches. Myxoma and hog cholera viruses were present in the bloody gut contents of infected leeches but were not demonstrable in the body tissues of these leeches. It seems from the findings presented that leeches are not biological carriers of either myxoma or hog cholera virus but instead carry these two agents mechanically in their gastrointestinal tracts. In doing this, they appear to protect the viruses from various deleterious chemical and physical influences to which they would have been exposed in the open. It is speculated that leeches could play a role in nature in perpetuating the blood-borne viruses of certain diseases in which close association with bodies of fresh water is of epidemiological importance.

Animals↗
PubMed1955

The swine lungworm as a reservior and intermediate host for swine influenza virus. V. Provocation of swine influenza by exposure of prepared swine to adverse weather.

Twenty-five swine, infested with lungworms infected with masked swine influenza virus, were exposed to adverse weather conditions on one or more occasions. Of these, 4 came down with apparent swine influenza, while 6 others developed serological evidence of infection with swine influenza virus. The remaining 15 prepared swine, as well as 8 lungworm-free control swine, failed to show evidence of swine influenza virus infection, despite repeated exposures to adverse weather. The data presented indicate that, in the 10 swine in which swine influenza virus infections were elicited, some feature of the weather to which the animals were exposed was responsible for provoking masked influenza virus to infectivity. The exact constituent of the meteorological complex comprising "weather", responsible for the provocation, cannot be determined from the data obtained.

Animals↗
PubMed1953

An antiviral substance from Penicillium funiculosum. I. Effect upon infection in mice with swine influenza virus and Columbia SK encephalomyelitis virus.

A culture of P. funiculosum isolated on Guam proved capable of elaborating a substance which exerted a favorable therapeutic effect against swine influenza virus infections in white mice. The culture was extremely variable and irregular in its production of the antiviral substance, and during maintenance in the laboratory for several years gradually lost this property. Efforts to restore it were unsuccessful. Subsequently it was found that the mold elaborated a substance, now designated helenine, which is therapeutically effective against Columbia SK encephalomyelitis virus infections in mice. Helenine appears to differ from the substance earlier procured from the mold, which was active against swine influenza virus infections in mice. It is frequently present in greater or lesser amount in the fluid portions of stationary cultures of P. funiculosum but is more regularly obtained and in larger amount, from the cellular components of the pellicles. When liberated from these latter by mechanical bruising and fracturing, it goes into solution in the culture fluids. It is precipitable from aqueous solution by 50 per cent acetone. Infected mice injected with helenine in amounts less than the amount which produces a maximal therapeutic effect exhibit a dosage response. Increasing the dose above the optimum fails to increase the therapeutic effect. Helenine exerts its maximum effect when given within the first 10 hours after viral infection but its influence is apparent even when treatment is delayed for up to 24 hours. It is not effective against massive amounts of virus and gives the best therapeutic results when used in the treatment of animals infected with from 10 to 1000 fatal doses of virus. Treatment of infected mice with helenine delays the entrance of virus into their brains for from 24 to 48 hours. The mechanism by which helenine exerts its therapeutic effect against SK virus is not known but the findings presented suggest either that it causes an inhibition or interruption of multiplication of the virus, slowing down the whole process of infection and spread to the central nervous system, or that in some way it interferes temporarily with the neuroinvasiveness of the virus.

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