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Biomedical subjects

D Collavo

Publications and source records attributed to D Collavo.

72 records · Page 4Linked to original sources
PubMed1975

In vivo interactions between murine leukemia and sarcoma viruses.

Experiments have been performed with the aim of elucidating the nature and the extent of the in vivo interactions between murine leukemia viruses (MuLVs) and murine sarcoma virus (MSV). BALB/c and CBA mice, injected neonatally with Graffi or passage A Gross viruses (MuLV-Gi, MuLV-G), have been inoculated as young adults with murine sarcoma virus, Moloney strain (MSV-M). A higher percentage of nonregressing sarcomas appeared in these animals, sometimes accompanied simultaneously by leukemia. The immune reactivity of mice receiving MuLV-Gi at birth was found to be significantly depressed when evaluated by the hemolytic palque-forming cell (PFC) technique. However, in mice infected with MuLV-Gi and MSV-M the number of PFC ranged within the control values or slightly increased. The potentiation of MSV-M oncogenicity following infection with MuLV was studied in a more natural situation. Adult AKR mice, known to release endogenous MuLV continuously, were injected with MSV-M. The incidence of induced sarcomas was similar to that observed in control BALB/c mice inoculated with MSV-M. Moreover, tumors developed with a very long latent period. On the other hand, the great majority of tumors showed no regression and ultimately killed the host. Additional experiments, making use of immunologic manipulation of the host and Fl hybrids, suggest that the relative resistance to MSV-M oncogenesis in AKR mice is influenced by genetic and immunologic factors. MSV recovered from MSV-M-induced tumors in AKR and C58 mice was typed by highly specific mouse antisera. The results clearly showed that formation of a new MSV pseudotype occurred in vivo, the endogenous Gross virus acting as helper.

AKR murine leukemia virus↗
PubMed1974

Tumor induction by murine sarcoma virus in AKR and C58 mice. Reduction of tumor regression associated with appearance of Gross leukemia virus pseudotypes.

Adult AKR and C58 mice injected intramuscularly with murine sarcoma virus, Moloney isolate (M-MSV), developed high incidence of nonregressing local tumors. Histologically, these tumors revealed the typical pleomorphism of M-MSV sarcomas; in some cases, however, neoplastic tissue showed a nodular or diffuse growth of monomorphic myoblastlike cells, reminiscent of clonal aggregates. No depression of immune reactivity was found in M-MSV-injected mice as evaluated by direct hemolytic plaque-forming cells against SRBC and by virus-neutralizing antibody production. The MSV recovered from the induced tumors proved to be, by neutralization assay, a Gross (G)-MSV pseudotype. Moreover, tumor cell suspensions absorbed out cytotoxic antibody directed against G-cell surface antigens. Therefore, the conclusion was drawn that MSV with envelope characteristics of endogenous G leukemia virus had formed in vivo through a phenotypic mixing phenomenon. The failure of tumors to regress has been interpreted as mainly due to the partial unresponsiveness of host immune reactivity towards G-MuLV specified antigens. Since MSV-tumors arose in AKR mice after a very long latent period, the possibility was considered that this relative resistance might depend on immunologic mechanisms. In fact, M-MSV-injected AKR mice immunodepressed by goat antimouse lymphocyte serum or rendered partially tolerant by neonatal M-MuLV inoculation developed sarcomas with higher incidence and with a shorter latency. Furthermore, the MSV recovered from these early tumors proved to be the original Moloney pseudotype.

AKR murine leukemia virus↗
PubMed1973

Prevention of murine sarcoma virus oncogenesis in offspring of immunized female mice.

BALB/c mice born to and nursed by females immunized against MSV-M showed a reduced tumour incidence and a high tumour regression rate following MSV-M injection at 7-14 days of age. Females immunized long before mating could also confer protection to their offspring whereas females immunized after parturition could not. A reduced number of tumours was observed in 3 out of 14 MSV-M injected litters whose mothers had been previously exposed to the virus while nursing infected offspring. Sera from suckling mice born to and nursed by immunized mothers contained MSV-M neutralizing antibody as shown by an in vitro focus reduction assay. Cell-free extracts from mice which developed leukaemia after MSV-M inoculation were tested for oncogenic activity in 1-week old mice. Out of 6 extracts, 4 induced typical MSV-M tumours and 2 caused leukaemias.

Animals↗
PubMedDate not supplied

[Histopathologic and ultrastructural study of tumors induced by murine sarcoma virus (msv) (author's transl)].

Various growth phases of Moloney murine sarcoma virus (M-MSV) induced tumors in suckling and young adult BALB/c mice have been studied by light and electron microscopy. In the early phase (3-6 days following M-MSV), observations at the injection site of the thigh muscles consisted of endo- and perimysial edema "activated" muscle satellite, cells, endothelial cells and fibroblasts, scattered type C virus particles within the muscle fibers, muscle fibers and endomysial cells undergoing necrosis and macrophage and granulocyte infiltration. During the overt tumor phase (6-12 days following M-MSV), observation of neoplastic tissue disclosed proliferation of several cell type (endothelial, periosteal, fibroblasts, etc.), poorly differentiated myoblasts along with atypical rhabdomyoblast-like cells and sarcolytes, type C virus budding from muscle fiber and myoblast plasma membrane, and intense degenerative and regenerative changes in the muscle fibers together with more profuse granulocyte infiltration. The regressive phase (13-21 days following M-MSV) presented reduced cellularity of the neoplastic tissue, a decrease in blast cells, diminishing granulocyte infiltration with contemporaneous appearance of prominent lymphocyte foci and gradual disappearance of virus particles. Although many cell types of mesenchymal origin proliferate following M-MSV infection, the above morphological findings indicate that striated muscle is a preferential site for virus replication and transformation. Furthermore, the peculiar virus cell relationships leading to cell lysis and continuous recruitment of newly infected cells have been widely documented. In the light of these findings it is suggested that, besides the host immune control of virus spread and tumor cell multiplication, the non clonal growth pattern of M-MSV induced tumors is a crucial factor in determining the spontaneous regression which occurs with high frequency in this experimental system.

Animals↗
PubMedDate not supplied

[Evidence of an intrinsic defect of lymphocyte reactivity in AKR mice (author's transl)].

Like their AKR/J parent, (CBAT6T6 X AKR/J)F1 mice are carriers of endogenous G-MuLV and present a high incidence of spontaneous lymphoma. However, the F1 hybrids do not present the immunological deficits seen in pre-leukemic AKR/J mice since they respond normally to in vitro PHA stimulation and to in vivo LPS immunization. These observations suggest that there is probably no direct relationship between the presence of MuLV and immunological impairment. Studies have been carried out to ascertain whether the altered immunological reactivity seen in AKR/J mice is related to factors intrinsic to the immunocompetent cells or to environmental inadequacy. Thus, (CBAT6T6 X AKR/J)F1 mice were thymectomized, irradiated, reconstituted with syngeneic bone marrow and simultaneous transplant of CBAT6T6 and AKR/J thymus, and their lymphocyte response to PHA was assayed. In addition, antibody production following LPS immunization was studied by transferring AKR/J splenic cells to irradiated CBA6T6 or (CBAT6T6 X AKR/J)F1 mice, and vice-versa. The results of these investigations indicate that an intrinsic lymphocyte hyporeactivity is present in AKR/J mice and environmental factors do not modify the reactivity of the transferred immunocompetent cells.

Animals↗
PubMedDate not supplied

Lymphokine-induced cytotoxic cell generation in thymus and spleen cell cultures.

The effect of a supernatant (SN-A) obtained from PMA-stimulated IL-2 producing EL-4 cells on cytotoxic cell induction in thymocyte and splenocyte cultures was evaluated. SN-A, but not recombinant IL-2 alone, induced cytotoxic cell differentiation in thymus cell cultures, thus indicating that factors distinct from IL-2 are required for effector cell generation. INF-gamma takes part in the process, and Ia+ accessory cell presence is also strictly required in thymus cultures for lymphokine-induced cytotoxic cell generation. Cytotoxic activity in thymocyte cultures was due only to Thy 1+ Lyt 2+ cells having a broad spectrum of target cell specificity, while in spleen cell cultures an effector population with NK activity was also generated.

Animals↗