Day Of Virus Inoculation Research Articles

Successful transplantation of Friend virus-induced preleukemia into stem cell-deficient fetal mice

The leukemias induced by the Friend polycythemia virus and other leukemogenic retroviruses have previously not been transplantable until weeks or months after virus inoculation. Because tumor-specific immune mechanisms persist in both irradiated and nude mice, it has not been possible to determine if this result is due to rejection of cells already immortalized by retrovirus infection, or reflects an inherent limitation in the proliferative capacity and malignancy of these “preleukemic” cells. To clarify these issues, we have transplanted virus-infected bone marrow into mouse fetuses that are immunologically immature and thus incapable of graft rejection. We report here that within days of virus inoculation, transplantable cells capable of disease progression in certain fetal hosts can be detected with this technique. These results demonstrate that cells with the capacity for extensive leukemic proliferation arise very early in Friend virus- induced disease. However, successful transplantation was seen only in genetically anemic recipients (Wx/Wv), which are deficient in hematopoietic stem cells, and not in their normal littermates. Thus, in accord with recent in vitro observations, this in vivo data suggests that normal hematopoietic cells, independent of immune mechanisms, can suppress the malignant progression of transformed cells.

Successful Transplantation of Friend Virus-Induced Preleukemia Into Stem Cell-Deficient Fetal Mice

The leukemias induced by the Friend polycythemia virus and other leukemogenic retroviruses have previously not been transplantable until weeks or months after virus inoculation. Because tumor-specific immune mechanisms persist in both irradiated and nude mice, it has not been possible to determine if this result is due to rejection of cells already immortalized by retrovirus infection, or reflects an inherent limitation in the proliferative capacity and malignancy of these "preleukemic" cells. To clarify these issues, we have transplanted virus-infected bone marrow into mouse fetuses that are immunologically immature and thus incapable of graft rejection. We report here that within days of virus inoculation, transplantable cells capable of disease progression in certain fetal hosts can be detected with this technique. These results demonstrate that cells with the capacity for extensive leukemic proliferation arise very early in Friend virus-induced disease. However, successful transplantation was seen only in genetically anemic recipients (Wx/Wv), which are deficient in hematopoietic stem cells, and not in their normal littermates. Thus, in accord with recent in vitro observations, this in vivo data suggests that normal hematopoietic cells, independent of immune mechanisms, can suppress the malignant progression of transformed cells.

Acyclovir therapy of neonatal herpes simplex virus type 2 infections in rabbits.

New Zealand white rabbits less than 30 h old were inoculated subcutaneously with 10(3) 50% tissue culture infectious doses of type 2 herpes simplex virus. The animals were randomly assigned to a treatment schedule of daily intraperitoneal injections of acyclovir, beginning on the day of virus inoculation for 6 or 12 days, on post-inoculation day 1 for 6 days, or on post-inoculation day 2 for 6 days. The acyclovir was given in doses of 50 mg/kg of body weight per day. Similarly infected animals receiving daily intraperitoneal injection of Eagle minimum essential medium served as controls. All of the control animals died on day 4 or 5 after inoculation. At death they exhibited severe skin lesions, viremia, and dissemination of virus in various visceral organs and spinal as well as trigeminal ganglia. In contrast, animals treated with acyclovir failed to develop significant skin lesions, and death did not occur while treatment continued. Termination of treatment after 6 days resulted in late-onset fatal disease and virus isolation from the brain in many rabbits regardless of the treatment schedule. No such late fatality was observed and no virus could be detected from the brain when treatment was initiated on the day of virus inoculation and continued for 12 consecutive days. With respect to all of the variables studied, treatment for 12 days beginning on the day of virus inoculation was most effective.

Protection and therapy of mice with acute and chronic experimental virus infections with propionibacterium granulosum KP-45

The protection of mice against experimental infections with three different viruses (herpes simplex, vaccinia and mouse hepatitis) by Propionibacterium granulosum strain KP-45 and isolated cell walls was investigated. Pretreatment of NMRI mice with P. granulosum strain KP-45 3-7 days prior to HSV intranasal infection resulted in lowering of mortality rate (herpes encephalitis) from about 95% in controls to 15-30%. Pretreatment of NMRI mice prior to vaccinia virus infection also caused a significant decrease of the number of specific tail lesions. Infection of BALB/c mice with mouse hepatitis virus type 3 (MHV-3) resulted in development of acute infection with lethality in 4-6 days, while in fairly resistant C3H mice chronic infection manifested by loss of weight, uncoordination followed by paralysis and death in few months was observed. Pretreatment of BALB/c mice 3-7 days prior to MHV-3 infection lowered the mortality rate to about 25-30% while no effect was observed in animals injected with P. granulosum KP-45 on the day of virus inoculation. In chronic MHV-3 infections treatment with P. granulosum KP-45 was started 2 weeks after virus inoculation and was continued every 10 days. This resulted in a significant lowering of the number of paralysed mice and in a decrease of the mortality rate. Titre of MHV-3 recovered from livers of infected mice 4 months after virus inoculation was also significantly lower in animals treated with P. granulosum KP-45 or isolated cell walls.

AN AVIAN LEUCOSIS GROUP-SPECIFIC COMPLEMENT FIXATION REACTION. APPLICATION FOR THE DETECTION AND ASSAY OF NON-CYTOPATHOGENIC LEUCOSIS VIRUSES.

Abstract Sera of hamsters bearing large primary or transplanted subcutaneous fibrosarcomas induced by the Schmidt-Ruppin (S-R) strain of Rous sarcoma virus contain complement-fixing (CF) antibodies reactive not only with the homologous virus, but also with antigens of other avian leucosis viruses. Using this group-specific reaction, a complement fixation test (the COFAL test) was developed for the specific detection and assay of viruses of the avian leucosis group; the test appears to be at least as sensitive and useful as the resistance-inducing factor (RIF) interference procedure. Virus was assayed by inoculating decimal dilutions of virus into chicken embryo fibroblast cultures grown in petri dishes or in roller tubes and testing the inoculated cultures for the development of CF viral antigens. End points for virus assays were obtained in petri dish cultures after one or two cell transfers and also in roller tube cultures without cell transfers. In both systems, virus diluted 10−4 to 10−5 was detected within 10 days of virus inoculation and final titration end points were often reached within 2 weeks. Rous-associated virus (RAV) was readily demonstrated in the Bryan strain but not in the S-R strain of Rous sarcoma virus. The test was effective in demonstrating naturally occurring avian lymphomatosis virus.