Studies of immune responses during recovery from Sindbis virus encephalitis in selectively reconstituted, thymectomized, lethally irradiated mice

Recovery from acute Sindbis virus encephalitis was studied in selectively reconstituted, thymectomized, irradiated mice. Intact mice cleared virus from the brain by day 10 and developed inflammation along with immunoglobulin M (IgM) and IgG antibodies 4 to 6 days after infection. Unreconstituted mice died by day 11, with virus still present but decreasing, no detectable antibody, and no evidence of inflammation. Mice reconstituted with bone marrow cells alone produced only IgM antibody and no inflammation, but cleared virus by day 14. Mice reconstituted with sensitized T cells alone cleared virus by day 10, produced very small amounts of antibody, and developed a prompt inflammatory response.

[1]  R. Hirsch Natural killer cells appear to play no role in the recovery of mice from Sindbis virus infection. , 1981, Immunology.

[2]  F. Liew,et al.  Differential sensitivity to cyclophosphamide of helper T cells for humoral responses and suppressor T cells for delayed‐type hypersensitivity , 1980 .

[3]  D. O. White,et al.  Further characterization of natural killer cells induced by Kunjin virus. , 1980, The Australian journal of experimental biology and medical science.

[4]  R. Fitzgeorge,et al.  The responses of normal an athymic mice to infections by togaviruses: strain differentiation in active and adoptive immunization. , 1980, The Journal of general virology.

[5]  R. Arnon,et al.  Effect of cyclophosphamide on suppressor cell activity in mice unresponsive to EAE. , 1979, Journal of immunology.

[6]  R. Hirsch,et al.  The pathogenesis of Sindbis virus infection in athymic nude mice. , 1979, Journal of immunology.

[7]  R. Hirsch,et al.  The effect of complement depletion on the course of Sindbis virus infection in mice. , 1978, Journal of immunology.

[8]  F. Ennis,et al.  The importance of an intact complement pathway in recovery from a primary viral infection: influenza in decomplemented and in C5-deficient mice. , 1978, Journal of immunology.

[9]  D. O. White,et al.  Two cytotoxic cells in peritoneal cavity of virus-infected mice: antibody-dependent macrophages and nonspecific killer cells. , 1977, Journal of immunology.

[10]  A. Ammann,et al.  Quantitation of B cells in peripheral blood by polyacrylamide beads coated with anti-human chain antibody. , 1977, Journal of immunological methods.

[11]  D. Griffin,et al.  Role of the immune response in recovery from Sindbis virus encephalitis in mice. , 1977, Journal of immunology.

[12]  I. Gresser,et al.  Role of interferon in the pathogenesis of virus diseases in mice as demonstrated by the use of anti-interferon serum. I. Rapid evolution of encephalomyocarditis virus infection , 1976, The Journal of experimental medicine.

[13]  F. Loor,et al.  T lineage lymphocytes in nude mice born from homozygous nu/nu parents , 1976, European journal of immunology.

[14]  V. Stollar Immune lysis of Sindbis virus. , 1975, Virology.

[15]  W. Tompkins,et al.  DESTRUCTION OF VIRUS-INFECTED CELLS BY ANTIBODY AND COMPLEMENT , 1975 .

[16]  J. Ziegler,et al.  Fatal echo 30 virus infection and amyloidosis in X-linked hypogammaglobulinemia. , 1975, Clinical immunology and immunopathology.

[17]  J. Trentin,et al.  Differential effects of cyclophosphamide on the B and T cell compartments of adult mice. , 1973, Journal of immunology.

[18]  H. McFarland,et al.  SPECIFICITY OF THE INFLAMMATORY RESPONSE IN VIRAL ENCEPHALITIS , 1972, The Journal of experimental medicine.

[19]  M. Oldstone,et al.  Acute viral infection: tissue injury mediated by anti-viral antibody through a complement effector system. , 1971, Journal of immunology.

[20]  A. Kark,et al.  Thymectomy in the adult mouse. , 1971, Transplantation.

[21]  B. Burke,et al.  Impaired Cellular Resistance to Herpes-Simplex Virus in Wiskott-Aldrich Syndrome , 1965 .