Hepatitis A virus.

The role of interferon in the pathogenesis of encephalomyocarditis (EMC) virus infection was determined by treating mice with potent, partially purified sheep anti-mouse interferon globulin. In control mice, EMC virus was present in low titers in various visceral organs but attained high titers in the brain towards the 4th to 5th day, at which time mice died with signs of central nervous system disease. In mice treated with anti-mouse interferon globulin, virus was present in high titer in visceral organs 24--36 h after viral inoculation and virtually all mice were dead by 45 h. This rapid evolution of EMC virus infection was not observed in mice treated with the globulin fraction prepared from a normal sheep, from a sheep exhibiting a low anti-mouse interferon-neutralizing titer, nor from a sheep having a high titer of antibody to human leukocyte interferon. The experimental results indicated that anti-interferon globulin neutralized the interferon liberated by virus-infected cells, thus permitting extensive virus multiplication in several visceral organs. We conclude that interferon is an important early component of host resistance to this virus infection.

In mice as demonstrated by the use of anti-interferon serum. I. Rapid evolution of encephalomyocarditis virus infection.

Role of target histocompatibility antigens in regulation of natural killer activity: a reevaluation and a hypothesis1

Resistance to malignant erythropoiesis induced by Friend spleen focus-forming virus and resistance to marrow stem cell allografts are under genetic control. Strains of mice, e.g., C57BL/6 and B10.D2, which are homozygous for resistance at the Fv-2 locus, are also good rejectors of most bone marrow allografts. 89Sr, a bone-seeking isotope, irradiates marrow but not other lymphoid organs and abrogates resistance to marrow allografts without suppressing T- or B-cell functions. Thus, marrow-dependent effector cells (M cells) seem to resist allogeneic stem cells. To test if the genetic resistance to Friend virus (FV) is also mediated by M cells, B6 mice were treated with 89Sr using a dosage schedule known to abrogate resistance to allogeneic marrow cells. 9 days after FV infection of such mice, the spleens showed malignant erythroblastosis which could not be suppressed by prior hypertransfusion, a procedure which suppresses physiologic erythropoiesis. Such 89Sr-treated B6 mice also supported extensive virus replication, while control mice did not. FV markedly suppressed the ability of 89Sr-treated B6 mice to produce antisheep red blood cell (SRBC) antibodies, a feature seen normally only in genetically susceptible mice. Thus, 89Sr-treated B6 mice behaved in these respects as if they were susceptible to FV. When increasing doses of 89Sr were administered to B6 mice, a dose-related loss of resistance to FV was seen. Therefore, it appears that 89Sr-sensitive M cells mediate the genetic resistance to FV. The results of experiments with 89Sr indicated that genetically resistant mice would be expected to possess target cells which are susceptible to transformation by FV. To verify this corollary, bone marrow cells from B10.D2 (Fv-2rr) mice were transplanted into previously infected and lethally irradiated DBA/2 (Fv-2ss) recipients which share the same H-2d alleles. 5–15 days later, the spleens of DBA/2 primary recipients yielded transformed cells which were capable of producing splenic tumor colonies upon transplantation into adult, unirradiated B10.D2 secondary recipients. Various control experiments clearly indicated that the tumor colonies so induced were of B10.D2 marrow origin. This indicated that B10.D2 stem cells could be transformed when allowed to interact with FV in the spleens of susceptible DBA/2 mice. However, 30 days after transplantation of B10.D2 bone marrow cells into DBA/2 recipients, no transformed cells were detected. Apparently, in the 30-day interval precursors in the B10.D2 marrow gave rise to mature M cells which resisted the leukemic process. Since M cells recognize hybrid or hemopoietic histocompatability antigens expressed on primitive normal and transformed hematopoietic cells, we suggest that M cells may exert surveillance by rejecting leukemic cells. Thus, marrow transplantation from genetically resistant donors may provide a new mode of treatment for leukemia, by providing precursors of M cells and other immunocompetent cell types.

Mechanisms of genetic resistance to friend virus leukemia in mice. I. Role of $sup 89$Sr-sensitive effector cells responsible for rejection of bone marrow allografts

Mechanisms of viral inhibition by interferons

Genetically Controlled Resistance to Flavivirus and Lactate-Dehydrogenase-Elevating Virus-Induced Disease.- Resistance to Herpes Simplex Virus - Type 1 (HSV-1).- Inborn Resistance of Mice to Orthomyxoviruses.- Role of Macrophages and Interferon in Natural Resistance to Mouse Hepatitis Virus Infection.- Genetic Resistance to Friend Virus-Induced Erythroleukemia and Immunosuppression.- Natural Cell-Mediated Immunity During Viral Infections.- Surveillance of Primitive Cells by Natural Killer Cells.- Indexed in Current Contents.

Natural resistance to tumors and viruses

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Natural resistance to tumors and viruses