Human parainfluenza virus type 3 inhibits gamma interferon-induced major histocompatibility complex class II expression directly and by inducing alpha/beta interferon.

摘要: Human parainfluenza virus type 3 (HPIV3) is one of the major causes bronchiolitis, pneumonia, and croup in newborns infants. Cellular immunity involving histocompatibility complex (MHC) class I II molecules plays an important role controlling infection. Several viruses have been shown to down-regulate gamma interferon (IFN-γ)-mediated MHC expression. In this communication, we show that HPIV3 strongly inhibits IFN-γ-induced expression HT1080 human fibrosarcoma cells. The culture supernatant HPIV3-infected cells also inhibited expression, a phenomenon was found be due, large part, alpha/beta (IFN-α/β). Expression intercellular adhesion molecule 1 occurred efficiently simultaneously infected with treated IFN-γ, indicating inhibitory effect specific II. STAT1 activation not affected by at early postinfection times but partially later times. These data suggested potent inhibition was, due defect downstream pathway. Class transactivator (CIITA) unique mediator transcription from promoter. By RNase protection analysis, CIITA containing IFN-α/β, on other hand, without affecting indicate primarily viral gene products targeting additionally inducing IFN-α/β target or more steps further downstream.