Induction of SOCS-3 gene transcription by viruses was reported for HSV-1, HCV [31] [32] [33] and for respiratory viruses, such as SARS and RSV [34, 35] . The level of induction of SOCS-3 by HSV-1 seems to determine whether infection turns to acute or persistent progression [31] . For HCV it has been suggested that upregulation of SOCS-3 may contribute to the non-responsiveness of HCV patients to IFN therapy [33, [36] [37] [38] . Elevated SOCS-3 mRNA levels during RSV infection were linked to Th2 cell-mediated immune disease as atopic dermatitis and asthma [39, 40] .