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Biomedical subjects

M A Basombrío

Publications and source records attributed to M A Basombrío.

34 records · Page 2Linked to original sources
PubMed1978

Active immunization against murine radiation-induced leukemia using a sarcoma virus pseudotype.

Immunization of C57BL/Ka mice against the radiation leukemia virus (Rad LV) markedly reduced their susceptibility to development of leukemia after X-radiation. The active immunogen used consisted of a sarcoma virus pseudotype of Rad LV which induces regressing sarcomas in young adult mice. These immunized animals were challenged with four weekly 160-rad X-ray exposures. The appearance of lymphomas and leukemias resulting from such irradiation was delayed and their incidence significantly decreased. These results indicate that oncornavirus immunization may be used to reduce the incidence of murine leukemias which are triggered by a physical agent.

Animals↗
PubMed1978

Murine leukemia virus in chemically-induced sarcomas as detected by XC plaque formation.

To detect whether methylcholanthrene induced murine sarcomas contain endogenous murine leukemia viruses, direct XC syncytium assays were performed over short term tumor cultures. Out of 31 sarcomas, 13 (42%) induced more than 4 plaques per flask, while no such activity was found in 39 control spleen samples. It is postulated that the positive tests are related to an increase in the titer of endogenous B-tropic virus, probably as a result rather than as a cause of tumor induction by chemicals.

Animals↗
PubMed1977

Enhanced growth of syngeneic Moloney sarcoma with decreased immunity in the regressors.

S.c. cellular transplants of MS tumours have a high incidence of rejection in adult BALB/c mice, which can then be used as syngeneic regressors. When these tumours were inoculated within a glass cylinder which had been implanted s.c. in BALB/c mice 2 days earlier, 51% of the animals died with progressively growing tumours, compared with 2% in animals which had received the same inoculum directly s.c. This experimental model demonstrates tumour enhancement in a syngeneic system, and duplicates what has been previously reported in two different allogeneic tumour-host combinations, where it was demonstrated that immunological enhancement was operating, since the addition of either progressor serum or soluble tumour antigen significantly increased tumour incidence. For the purpose of investigating whether the glass cylinder model could also modify the immune response of the host to a second tumour challenge, a leukaemia virus known to crossreact with MS was used. Regressors were challenged i.p. with a lethal dose of a leukaemia virus, PLLV. Regressors bearing a glass cylinder showed a 22% survival rate which was significantly lower than that of the s.c. inoculated regressors (71%). This decrease in cross-immunity suggests that the artificially constructed privileged site created by the glass cylinder, by conditioning for tumour enhancement, also decreases immunological memory.

Animals↗
PubMed1977

Murine sarcoma virus pseudotypes used as immunogens against viral and chemical oncogenesis.

The purpose of this study was to develop an animal system of protective immunity against oncornaviruses and to test whether such immunization had an inhibitory effect upon chemical sarcomagenesis. Several murine sarcoma virus (MSV) pseudotypes were used as immunogens and tested against themselves, against other pseudotypes, against leukemogenesis by their helper viruses, and against sarcomagenesis by 3-methylcholanthrene. Five MSV pseudotypes were obtained by rescuing complete MSV from MSV-genome carrier, nonproducer hamster tumor cells, using five different leukemia viruses as helpers. The immunogenic properties of these pseudotypes could be specified on the basis of the following observations. 1) They all induced sarcomas in newborn mice and regressing sarcoma nodules in young adult mice. After regression, most mice remained free of neoplastic disease, but some developed sarcoma or leukemia relapses. 2) They had an individual host range pattern, usually determined by the helper virus, as tested by inoculation of a constant virus dose in BALB/c, C57BL/Ka, and Swiss mice. 3) They were all immunogenic, in the sense that the first virus inoculation prevented sarcoma induction by a second challenge, either viral or cellular. 4) They were cross-reactive in vivo, one pseudotype immunizing against another, in the combinations tested. 5) They were able to immunize against leukemogenesis induced by their helper viruses. This was shown by prevention of leukemic deaths by Rauscher and Friend viruses, by a slight prolongation of survival after challenge with the Precerutti-Law leukemia virus, and by inhibition of splenomegaly by Moloney leukemia virus. In a second stage of the study, we investigated whether immunization with any of the MSV psuedotypes had an inhibitory effect upon sarcomagenesis induced by near-threshold doses of 3-methylcholanthrene. The incidence of these sarcomas was essentially the same in virus-immunized and control mice. It was concluded that immunizing procedures able to prevent sarcomagenesis when the inducer is a virus did not have any consistent preventive effect when the inducer was a chemical.

Animals↗
PubMed1976

Effect of a Rauscher leukemia virus vaccine upon chemical oncogenesis in the mouse.

The concept that type-C RNA viruses serve as determinants of chemically induced cancer would be supported if immunization against such viruses reduced the incidence of methylcholanthrene-induced sarcomas. A formalin vaccine was employed which was able to protect mice against the development of virus-induced Rauscher leukemia: 8/12 vaccinated mice survived versus 1/12 controls. When mice so immunized were challenged with near-threshold doses of chemical carcinogen, sarcoma incidence and death latency did not differ between vaccinated and control groups: within 10 months, a 320 mug dose of methylcholanthrene induced 100% sarcomas in both groups, while a 64 mug dose induced 62% and 65% tumors in vaccinated and control mice respectively. Thus, a relevant postulate of the oncogene hypothesis could not be supported by these studies. Formalin treatment neutralizes the oncogenic effect of mouse leukemia viruses yiwlding preparations that are immunogenic and can be successfully used as vaccines to protect against virus-induced leukemia (5). The finding of murine leukemia viruses in chemically induced tumors (1, 2) poses the question of whether these viruses are present in the tumors as passengers, or whether they are etiologically involved in the process of tumor induction. An approach to answering this question would be to challenge with chemical carcinogens mice which have been vaccinated with leukemia virus. If the virus were somehow involved in tumor induction, antiviral immunization might conceivably interfere with chemical carcinogenesis. Whitmire and Huebner (9) have reported that mice immunized with formalin-treated leukemia viruses, become resistant to sarcomagenesis by methylcholanthrene. Repetition of this experiment by Gericke and Chandra (6) gave non-significant differences between experimental and control groups. The present paper deals with the effect of immunization against Rauscher leukemia virus upon tumor induction by near-threshold doses of methylcholanthrene.

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PubMedDate not supplied

A cost-benefit analysis of Chagas disease control in north-western Argentina.

Chagas disease has been controlled in the Department of Anta, Province of Salta, Argentina, through a series of vector control interventions beginning in 1983. Based on data from this programme, together with estimates of the value of benefits accruing to the programme due to avoidance of new cases of Chagas disease, we present an analysis of costs and benefits of the vector control interventions. Under all assumptions, the interventions have been highly profitable from a societal point of view, with an internal rate of return in excess of 60%. The net present value of benefits accruing to the programme is estimated to be above US$7 million.

Acute Disease↗
PubMedDate not supplied

Complete immunization against Trypanosoma cruzi verified in individual mice by complement-mediated lysis.

Experimental systems to assay immunity against Trypanosoma cruzi usually demonstrate partial resistance without excluding the establishment of sub-patent infections in protected animals. To test whether Swiss mice immunized with attenuated parasites might develop complete resistance against virulent T. cruzi, experiments were performed involving challenge with low numbers of parasites, enhancement of local inflammation and the combination of natural and acquired resistance. Absence of infection was established after repeated negative parasitological tests (including xenodiagnosis and hemoculture), and lack of lytic antibody was tested by complement mediated lysis. Immunization with 10(7) attenuated epimastigotes conferred protection against the development of high levels of parasitemia after challenge with Tulahuen strain, but was unable to reduce the number of infected animals. However, when a strong, delayed-type hypersensitivity reaction was triggered at the site of infection by injecting a mixture of virulent and attenuated T. cruzi, a significant proportion of immunized animals remained totally free of virulent infection. The same result was obtained when the immunization experiment was performed in four month old Swiss mice, displaying a relatively high natural resistance and challenged with wild, vector-borne parasites. These experiments demonstrate that complete resistance against T. cruzi can be obtained in a significant proportion of animals, under conditions which replicate natural, vector delivered infection by the parasite.

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