POOR INDUCTION OF INTERFERON-INDUCED 2',5'-OLIGOADENYLATE SYNTHETASE (2-5-AS) IN CELLS PERSISTENTLY INFECTED WITH MUMPS-VIRUS IS CAUSED BY DECREASE OF STAT-1-ALPHA

Poor induction of interferon-induced 2',5'-oligoadenylate synthetase ( 2-5AS) has been demonstrated in cells persistently infected with mumps virus as compared with uninfected cells. As for the number of interfe ron (IFN) receptors and the level of IFN regulatory factors (IRF-1 and IRF-2) mRNAs, there was little difference between them. Therefore, it is suggested that the IFN-alpha signaling system is ineffective, in t he persistently infected cells. Components of IFN-stimulating gene fac tor 3 alpha (ISGF-3 alpha), STAT-1 alpha (p91) and STAT-2 (p113), were investigated in human amnion (FL), human nasopharyngeal cancer (KB), human T-lymphoid (HUT 78), and human B-lymphoid (Akata) cells persiste ntly infected with mumps virus. STAT-1 alpha, but mot STAT-2, disappea red in these persistently infected cells, and this factor was not rest ored by treatment of these cells with IFN. However, no difference was observed between the levels of STAT-1 alpha mRNA transcript in persist ently infected and uninfected control cells. It is reasonable to infer that the poor induction of 2-5AS activity is due to the decrease of S TAT-1 alpha in correlation with the IFN-signal transduction pathway. F urthermore, induction of other IFN-stimulated genes (ds-RNA activated protein kinase, PKR, and MxA protein) was also reduced in the cells pe rsistently infected with mumps virus.