Human lymphoblastoid cell lines transformed in vitro by the Epstein-Barr virus (EBV) had receptors for fixed complement detectable by a rosette test. EBV transformed cells derived from cotton-topped marmoset leukocytes did not express this receptor. Evidence is presented that both human and marmoset cell lines arose from precursor cells which have complement receptors. Our findings suggest that transformation of marmoset leukocytes by EBV results in the loss of a differentiated surface marker.
Dog thymus cells chronically infected with HL-23V, a C-type virus isolated from human acute myelogenous leukemia cells, produced both transforming and nontransforming virus indistinguishable from simian sarcoma virus type 1 (SSV-1/SSAV-1) and induced fibromas in newborn marmosets. All inoculated marmosets developed anti-HL-23V antibodies. A cell line established from a tumor biopsy produced transforming virus identical to SSV-1 and HL-23V at early passages. However, at later passages the cell line and a cell line established from residual tumor tissue removed at autopsy, produced virus which was neutralized only at low dilutions of anti-SSV-1 serum (1:32) relative to SSV-1 (1:1,024). This virus (BFV) was also distinguished from SSV-1 and HL-23V by XC tests, and by membrane immunofluorescence and serum cytotoxicity tests.
We find that colonic adenocarcinoma, which is an extremely rare neoplasm of all animals except man and carcinogen-treated rodents, occurs spontaneously in some marmosets. The cotton-topped Saguinus oedipus oedipus is particularly prone to develop it, but we have found it also at necropsy in Callimico goeldii (Goeldi's marmoset). Numerous metastases to regional lymph nodes develop. The cancers arise de novo in the mucosa and early invade the submucosa and lymphatic apparatus and paracolonic lymph nodes. These findings and the continuing occurrence of this cancer in our colony suggests that the marmoset may be the long-sought primate model for experimental intestinal carcinogenesis.
The various species of marmosets are susceptible to a wide variety of infectious agents of which only a few have been fully characterized. Little is known concerning spontaneous disease in their natural habitat, and often deaths in the laboratory go unexplained. In captivity, Herpesvirus-T infection appears to be the most important viral infection, but serious disease may also follow infection with measles virus (rubeola) and an unidentified paramyxovirus. Bacterial diseases are multiple, but rarely occur as epizootics. Various species of Salmonella, Yersinia, Klebsiella, and Diplococcus are among the more frequent pathogens. Mycoses and parasitic infections are also numerous, but most do not result in major losses.
The current and proposed colony design and management are described. In an effort to increase the neonatal survival of marmosets, an outdoor-indoor housing arrangement is planned.
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