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Biomedical subjects

M S Hirsch

Publications and source records attributed to M S Hirsch.

At least 235 records · Page 13Linked to original sources
PubMed1976

Hepatitis in an adult caused by Herpes simplex virus type I.

Disseminated infection caused by Herpes simplex virus (HSV) type I is described in a previously healthy adult. The clinical course was characterized by progressive hepatic failure, fever, hypotension, atypical lymphocytosis, and disseminated intravascular coagulation. No skin lesions were present and the causal agent was not suspended premortem; however, HSV-I was isolated from autopsy liver, and characteristic histopathological lesions of herpes infection were observed in liver and esophagus.

Aged↗
PubMed1975

Activation of C-type viruses during skin graft rejection in the mouse. Interrelationships between immunostimulation and immunosuppression.

Both mouse-tropic and zenotropic C-type RNA viruses were activated in BALB/c mice during rejection reactions against skin grafts from mice differing at the major histocompatibility locus (A/J) or sharing this locus (DBA/2). Animals that maintained their skin grafts following immunosuppression with antilymphocyte serum (ALS) or cyclophosphamide had a much higher incidence of virus-positivity than animals that did not receive ALS or cyclophosphamide, or that rejected their skin grafts despite immunosuppressive therapy. ALS itself activated type-C viruses from a small proportion of BALB/c mice whereas cyclophoshamide alone did not. Type C viruses were detected in spleens and regional nodes draining skin-graft sites between 1 and 2 weeks following transplantation; thereafter they reached maximum titers in spleens. Viruses were not detected at skin-graft sites, in tails or in thymuses of grafted animals. Virus activation was associated with splenic histological changes consisting of germinal center formation, diffuse hyperplasia of reticulum cells, depletion of periarteriolar lymphocytes and hyperplasia of red pulp hematopoietic elements.

Animals↗
PubMed1975

Immunological mechanisms in the pathogenesis of virus-induced murine leukemia. I. Autoreactivity.

By an in vitro microcytotoxicity assay, thymocytes from mice infected with Moloney murine leukemia virus since birth (MuLV-M carriers) caused a dramatic reduction of normal, non-infected syngeneic target cells; they usually spared identically derived target cells infected with MuLV-M. Thymocytes from normal mice slightly stimulated the replication of the same target cells. This pattern of carrier thymocyte reactivity was evident at all ages tested during both preneoplastic and neoplastic periods. Transplantable lymphoma cells derived from a carrier mouse with overt thymic lymphoma behaved similarly. Lymphocytes from the spleens and lymph nodes of young preleukemic carriers (8-12 weeks old) usually were reactive against MuLV-M-infected tarted cells and not against non-infected target cells. In contrast, lymphocytes from older preleukemic carriers (16-17 weeks old) reacted in a manner similar to carrier thymocytes. These observations suggest that the thymic lymphoma induced by MuLV-M may result in part from an autoreactive process originating in the thymus, but eventually spreading to the peripheral lymphoid tissues.

Animals↗
PubMed1975

Immunological mechanisms in the pathogenesis of virus-induced murine leukemia. II. Characterization of autoreactive thymocytes.

The nature of the reaction and the type of effector cells involved in the reactivity of thymocytes from Moloney murine leukemia virus (MuLV-M)-carrier mice against normal syngeneic target cells has been further characterized. The reaction is mediated by viable MuLV-infected thymocytes. Lysates of carrier thymocytes are not more effective in causing target cell reduction than are lysates of normal thymus cells. Soluble mediators do not appear to be involved in the reaction. The thymocytes mediating the reaction are non-adherent cells positive for the theta-C3H and H-2-k alloantigens, but are negative for detectable murine IgG determinants. Their resistance to corticosteroid treatment further identifies them as functionally mature immunocytes.

Animals↗
PubMed1975

Autoaggressive reactions and leukemia virus infections: interrelated events in their pathogenesis.

Leukemia viruses can be activated from within murine hosts by immunological reactions against foreign histocompatibility antigens both during graft versus host reactions (GVHR) and host versus graft reactions (HVGR). Presence of both lymphocyte-mediated graft rejection reactions and immuno suppression appears necessary for maximal virus activation and replication in vitro, although viruses can be activated by mixed lymphocyte reactions (MLR) alone in vitro. During HVGR, viruses are first detectable in lymph nodes draining the graft site, and later reach maximal titers in the spleen. Mice infected with murine leukemia virus (MuLV) as neonates or carrying MuLV secondary to milk transmission (carriers) also develop complex autoaggressive responses. By a sensitive in vitro microcytotoxicity assay, neoplastic or pre-neoplastic thymocytes from carrier mice were found to react vigorously against normal uninfected syngeneic embryonic fibroblasts, whereas they reacted much less vigorously with similarly prepared but MuLV-infected fibroblasts. Thymocytes from uninfected animals did not react with infected or uninfected fibroblasts. Peripheral lymphocytes from carriers reacted against MuLV infected fibroblasts, but not against uninfected fibroblasts, a pattern indistinguishable from deliberately-immunized mice. It is proposed that responses analogous to GVHR are also important in the pathogenesis of leukemia following exogenous leukemia virus infection.

Animals↗
PubMed1973

Murine leukemia: a virus-induced autoimmune disease?

Thymocytes from mice carrying Moloney murine leukemia virus since birth are cytotoxic for normal syngeneic fibroblasts; they are much less cytotoxic for the same cells infected with this virus. The cytotoxic thymocytes appear to increase in number with age of the carrier mice and are present both during preleukemic and leukemic periods. These results suggest that lymphomas in carrier mice result from a sequence of events initiated by intrathymic destruction of normal cells by virus-infected cells, and culminating in the unrestricted proliferation of autoaggressive clones in the thymic cortex.

Animals↗
PubMed1973

Leukemia virus activation during homograft rejection.

Activation of murine leukemia viruses, as detected by the mixed culture cytopathogenicity (XC) assay, followed the transplantation of A/J skin onto immunosuppressed BALB/c mice. Virus was found in most of the mice receiving both skin grafts and antilymphocyte serum, but not in animals receiving either the serum alone, skin graft alone, or no treatment.

Animals↗
PubMed1973

Immunological control of polyoma virus oncogenesis in mice.

Adult CBA mice thymectomized, treated with antilymphocytic globulin (ALG) and inoculated with human leprosy organisms were accidentally infected with polyoma virus and all developed tumours. After cessation of ALG administration, some animals were given spleen cells from syngeneic donors immunized with polyoma virus; none developed tumours. Similar results were obtained in mice deliberately infected with polyoma virus but not with leprosy organisms. Passive transfer of antibody before but not after virus inoculation prevented tumour formation in immunosuppressed recipients. Virus infection in thymectomized, lethally irradiated and bone marrow reconstituted mice resulted in only a very low incidence of tumours. These results emphasize the role of immunological surveillance in preventing polyoma tumour formation under natural conditions.

Adenocarcinoma↗