Is rodent virus contamination of monoclonal antibody preparations for use in human therapy a hazard?
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Animals↗
Biomedical subjects
P Carthew
Publications and source records attributed to P Carthew.
Mouse interferon produced in vivo does not inhibit the development of preimplantation mouse embryos.
Mouse embryos were cultured in vitro in medium with serum containing interferon which had been induced in vivo by intravenous administration of polyinosine-polycytidylic acid. Two-cell and blastocyst-stage embryos were incubated for 72 and 24 h respectively before embryo transfer, or fixation to determine cell number. Further, blastocysts were outgrown on coverslips in embryo culture medium with fetal calf serum and interferon. Expression of an intermediate filament protein (Mr 55 000) in blastocyst outgrowths was examined with a monoclonal antibody. Embryos appeared morphologically normal and after treatment the mean cell number did not differ from that of controls. Implantation was unaffected by any of the treatments, but culture before transfer in medium containing mouse serum reduced the number of normal fetuses recovered on Day 14 of gestation compared to those cultured in medium without serum. Exposure to interferon did not modify the expression of filaments in the outgrown blastocyst. It is therefore unlikely that interferon induced by viral infection during pregnancy is responsible for preimplantation embryonic loss.
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Pathogenicity of mouse hepatitis virus for preimplantation mouse embryos.
Mouse embryos which were hatched from the zona pellucida in vitro in the presence of mouse hepatitis virus (MHV) or outgrown on coverslips and then exposed to MHV were shown by immunohistochemical staining to have virally infected trophoblast cells. Zona-intact embryos incubated with MHV for 48 h (2-cell embryos) or 1.5 h (blastocysts) were resistant to infection. Morulae and early blastocysts collected from donor mice experimentally infected with MHV were not infected, but the medium in which they were flushed from the uterine horns was contaminated with virus. No virus was detected after embryos were washed through three changes of uncontaminated medium. MHV was transmitted to foster mothers when embryos were transferred in medium contaminated with the virus. Fetal and decidual tissues were not infected. We suggest that embryo transfer is an effective and simple alternative to Caesarian rederivation of MHV-contaminated mice.
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Histopathological characterization of the naturally occurring hepatotropic virus infections of nude mice.
In the last ten years the mutant athymic nude mouse has been used by many researchers as a model for studying pathological conditions in an immunodeficient host. A major problem with such mice is their susceptibility to viral infections indigenous to murine stocks, such as the hepatotropic mouse coronaviruses. In an effort to define the hepatotropic virus diseases indigenous to nude mice this paper details the pathogenesis and associated comparative histopathology of three common strains of mouse hepatitis virus, reovirus 3 and murine cytomegalovirus in the nude mouse.
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Elimination of Sendai (parainfluenza type 1) virus infection from mice by embryo transfer.
Preimplantation embryos collected from mice in the acute phase of Sendai virus infection were not infected. Transfer of embryos from infected donors did not transmit the virus to the recipient foster mothers or to their progeny. The pregnancies were normal with no differences in implantation rate or number of live births when compared with control transfers of embryos collected from non-infected donors.
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Therapeutic effect of acyclovir (ZoviraxTM) on the pathogenesis of chronic murine cytomegalovirus infection in the immunodeficient nude mouse.
The ability of acyclovir (ZoviraxTM) to influence the outcome of chronic cytomegalovirus infection in the nude mouse has been studied over a period of 3 weeks. Nude mice infected with a low dose of murine cytomegalovirus develop a chronic progressive disease which is characterized by typical lesions in the lung, the liver, salivary glands and many other organs. After 18-21 days most nude mice die of pneumonia and hepatitis. When acyclovir (ZoviraxTM) was administered s.c. twice daily, starting 1 day after the infectious dose of virus, a marked improvement was noted. No nude mice given the drug died in the 21-day period and the number of lesions to the lung, liver and salivary glands was reduced quantitatively by a highly significant amount.
Acyclovir↗
Inhibition of the mitotic response in regenerating mouse liver during viral hepatitis.
Viral hepatitis caused by infection with murine hepatitis virus strain A59 has been shown to affect the mitotic response after partial hepatectomy in mice. Normal mice showed a delayed response, whereas nude mice did not show any response, even 5 days after partial hepatectomy.
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Secondary infection of rat lungs with Pasteurella pneumotropica after Kilham rat virus infection.
Lung congestion was observed after an outbreak of Kilham rat virus infection (KRV) in a rat colony, previously free of all rat viruses. A high proportion of congested lungs contained Pasteurella pneumotropica suggesting that KRV might have caused primary damage to the alveoli (hitherto not recorded) which allowed the secondary bacterial colonization. Experimental infection of rats with KRV caused acute damage to the lung alveoli. Since KRV infection is very common in animal facilities it could therefore be a significant agent in the development of respiratory disease.
Animals↗
Diagnosis of sialodacryoadenitis virus infection of rats in a virulent enzootic outbreak.
In a natural outbreak of sialodacryoadenitis virus it was observed that the incidence of clinical signs in spontaneous-hypertensive rats was 100%, and that these signs were of a severity not observed before in other strains of rats. Rats free of the virus were introduced so that the progress of the disease could be studied under natural conditions of spontaneous spread from the enzootically-affected breeding colony. The pathogenesis of the infection in these Sprague-Dawley rats has been recorded over a period of 10 days after their introduction to the colony, and the results of extensive serological screening have shown that the antibody response of the spontaneous-hypertensive rats to the virus is lower than in other strains of rat.
Animals↗
Comparison of alkaline phosphatase and horseradish peroxidase conjugated antisera in the ELISA test for antibodies to reovirus 3, mouse hepatitis and Sendai viruses.
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Alkaline Phosphatase↗
Murine coronaviruses: the histopathology of disease induced by intranasal inoculation.
Mice inoculated intranasally with murine coronaviruses (mouse hepatitis viruses) were killed daily for seven days. Lung and liver sections stained by the immunoperoxidase technique indicated that with three of the four strains examined viral localisation and replication in the lung preceded that found in the liver. Thus, infection by the respiratory route may be of importance in the transmission of these viruses.
Animals↗
The pathogenesis of chronic viral hepatitis in the nude mouse and its influence on liver regeneration after partial hepatectomy.
The pathogenesis of chronic viral hepatitis due to infection with mouse hepatitis virus Type 1 has been followed over a period of 30 days in the nu/nu mouse. The initial histopathology is that of a focal hepatic necrosis which evolves into a chronic hepatitis with cirrhosis. The histopathology of the experimentally induced hepatitis with mouse hepatitis Type 1 is indistinguishable from that produced by the disease in nude mouse colonies due to the natural infection in the United Kingdom and also indistinguishable from the histopathology produced by the nude mouse hepatitis virus isolated in Japan. The virus produces a temporary suppression and delay in liver regeneration of nude mice which have been partially hepatectomized and this is compared to the delay in liver regeneration induced by another more virulent strain of mouse hepatitis, Type A59, in the nude mouse.
Animals↗
A comparison in germ-free mice of the pathogenesis of Sendai virus and mouse pneumonia virus infections.
The poathogenesis of Sendai virus and pneumonia virus of mice (PVM) was studied using the immunoperoxidase technique on paraffin lung sections. The pathology of Sendai virus corresponds to that of a bronchopneumonia, with virus demonstrated by immunoperoxidase in the bronchial epithelium, and sometimes in macrophages, for a period of 2--9 days post-infection. Pneumonia virus of mice produces an interstitial pneumonia with virus demonstrated in the bronchial epithelium but also in the alveolar walls and alveolar macrophages. This virus can be demonstrated between 2 and 7 days post-infection. This technique was used to demonstrate PVM in the case of a natural outbreak of this disease and may eventually become a routine technique for the screening of lung tissue for respiratory viruses.
Animals↗
Prevalence of indigenous viruses in laboratory animal colonies in the United Kingdom 1978-1979.
Compared with the results of the previous serological survey of 1976-1977, it can be seen that mouse hepatitis virus is still prevalent in the mouse colonies and that corona viruses of rats are also common. The prevalence of Sendai virus has increased considerably. However, the prevalence of Reo 3 virus appeared to have decreased, although this may be the results of the different test used.
Animals↗
Persistence of pneumonia virus of mice and Sendai virus in germ-free (nu/nu) mice.
The pathogenicity and persistence of pneumonia virus of mice (PVM) and Sendai virus has been studied using germ-free nu/nu mice. PVM was found to infect cells of the bronchial epithelium (and the alveolar wall) of the lungs of germ-free nu/nu mice using the immunoperoxidase technique. The virus was located in the bronchial epithelium for 11 days before elimination, but persisted in the alveolar wall for the duration of the experiment (20 days). After Day 10 a humoral antibody response to PVM was observed which persisted, although at a low level (1 in 40), by haemagglutination-inhibition (HI) testing. Sendai virus in nu/nu mice also infected cells of the bronchial epithelium and this persisted for the duration of the experiment (27 days). The persistence of virus in the bronchial epithelium in relation to lack of humoral antibody is discussed with reference to local secretory antibody production, especially since this does not occur with PVM.
Animals↗
Sendai virus in nude and germ-free rats.
The pathogenesis of Sendai virus infection was studied in athymic and AGUS rats. The infection was more severe in the athymic rats and caused considerable clinical disease. Virus was shown to replicate in the bronchial epithelium and persisted in athymic rats for the duration of the experiment (32 days). The characteristic changes of necrosis of the bronchial epithelium and subsequent hyperplasia also persisted in this group and was accompanied by quite extensive interstitial pneumonitis. The virus failed to evoke an antibody response in the athymic rats.
Animals↗
Immunoperoxidase technique for the rapid differentiation of murine enteric viruses in tissue culture.
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Animals↗