Infectious mononucleosis is caused by the Epstein-Barr virus (EBV), an unusual human pathogen because it preferentially infects B lymphocytes and consequently activates them to produce immunoglobulins. When cultures of lymphocytes from patients with infectious mononucleosis were stimulated with polyclonal activators, unseparated cells failed to produce immunoglobulins, whereas purified B cells responded normally. Cocultures demonstrated profound suppressor T-cell activity in blood from patients with infectious mononucleosis. Early in this disease, circulating immunoglobulin-secreting cells were elevated, but during the second week their number was strikingly depressed. These data indicate that during infectious mononucleosis, EBV causes polyclonal activation of B cells, reflected by hypergammaglobulinemia and increased circulating immunoglobulin-secreting cells. Next, suppressor T cells become activated and inhibit further B-cell activation. Thus, activation of suppressor T cells in infectious mononucleosis provides a unique additional mechanism of host defense because these T cells inhibit the activation and proliferation of an important target of the causative virus.
Antiangiogenic therapy using Semliki Forest virus ( SFV ) carrying Endostatin gene for malignant brain tumor was investigated to improve the therapeutic efficacy. The efficiency of SFV -mediated gene delivery was first evaluated for B 16 cells and compared with the efficiency in cells of endothelial origin ( HMVECs ). HMVECs are more susceptible to SFV infection than B 16 cells. For the in vivo treatment model, phosphate -buffered saline, SFV -LacZ, retrovirus vector GCsap -Endostatin, and SFV -Endostatin were injected to mice bearing B 16 brain tumors. A very significant inhibition of tumor growth was observed in the group that had been treated with SFV -Endostatin. A marked reduction of intratumoral vascularization was seen in the tumor sections from the SFV -Endostatin group compared with tumor sections from the SFV -LacZ or GCsap -Endostatin groups. Moreover, at day 7 after intravenous administration of SFV -Endostatin, the serum level of endostatin was augmented more than 3 -fold compared to that after intravenous administration of GCsap -Endostatin. The results indicated that treatment with SFV -Endostatin inhibited the angiogenesis with established tumors. Gene therapy with Endostatin delivered via SFV may be a candidate for the development of new therapy for brain tumors. Cancer Gene Therapy ( 2001 ) 8, 796 -802
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