Suppressed Induction of 2‐5AS in Cells with HTLV‐I Is Not Associated with the Fluctuation of IFN‐Receptor, IFN‐Regulatory Factors (IRF‐1 and IRF‐2) or STAT‐1α

Abstract

Some viruses seem to be capable of suppressing interferon (IFN)-induced 2', 5'-oligoadenylate synthetase (2-5AS) induction. Cells infected with human T-lymphotropic virus type-I (HTLV-I) show different natures for the constitutive production of IFN-'y or sensitivity to IFN. Poor induction of 2-5AS was found in IFN-'y producer cells carrying HTLV-I (MT-1, MT-2 and SMT-1). On the other hand, in non-or low-producing cell lines of IFN-7 such as HUT102 and OKM-2, significant activity of 2-5AS was induced by treatment with IFN-a. A satisfactory level of IFN receptor was detectable in SMT-1 cells in spite of the poor induction of 2-5AS. There were no differences in either the interferon regulatory factor-2 (IRF-2) mRNA transcript or the level of STAT-la between SMT-1 and HUT102 cells. However, the transcription of IRF-1 mRNA was slightly reduced in SMT-1 cells as compared with that of HUT102 cells.

Human T-cell leukemia virus type 1 blunts signaling by interferon alpha

“…The lack of HTLV-1 inhibition of IFN-α-stimulated IRF1 expression suggests that cell surface presentation of IFN-αR1 and IFN-αR2 and IFN-α binding is not perturbed by HTLV-1. This is consistent with a previous report (Yokosawa et al, 1997). Immunoblot studies showed that HTLV-1 did not have an effect on total JAK1, TYK2, STAT1 and STAT2 protein levels ( Fig 5).…”