Abstract

Several viruses are known to infect human liver and cause the hepatitis, but the interferon (IFN) response, a first-line defense against viral infection, of virus-infected hepatocytes is not clearly defined yet. We investigated innate immune system against RNA viral infection in immortalized human hepatocytes (HuS-E/2 cells), as the cells showed similar early innate immune responses to primary human hepatocytes (PHH). The low-level constitutive expression of IFN-α1 gene, but not IFN-β and IFN-λ, was observed in both PHH and HuS-E/2 cells in the absence of viral infection, suggesting a particular subtype(s) of IFN-α is constitutively produced in human hepatocytes. To examine the functional role of such IFN-α in the antiviral response, the expression profiles of innate immune-related genes were studied in the cells with the treatment of neutralization against type I IFN receptor 2 (IFNAR2) or IFN-α itself to inhibit the constitutive IFN-α signaling before and after virus infection. As the results, a clear reduction of basal level expression of IFN-inducible genes was observed in uninfected cells. When the effect of the inhibition on the cells infected with hepatitis C virus (HCV) was examined, the significant decrease of IFN stimulated gene expression and the enhancement of initial HCV replication were observed, suggesting that the steady-state production of IFN-α plays a role in amplification of antiviral responses to control the spread of RNA viral infection in human hepatocytes.

Highlights

  • It has been shown that the replication of RNA viruses, including Sendai virus (SeV), Vesicular stomatitis virus, Newcastle disease virus, Sindbis virus, and Hepatitis C virus (HCV) is suppressed by type I interferon (IFN) (IFN-a and IFN-b) produced rapidly from the cells after infection of viruses [1,2]

  • We examined the antiviral responses of IFN system in some human hepatocyte derived cells against RNA viral infection using sendai virus (SeV) which is a negative strand RNA virus and has been widely used in studies on induction of IFN system [13]

  • We showed that IFN-a1 gene is expressed in HuSE/2 cells without virus infection as in the case of primary human hepatocytes (PHH), albeit at a low level and that the IFN-a, including IFN-a1, functions to elevate the expression of the genes related with anti-viral innate immune system in the cells

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Summary

Introduction

It has been shown that the replication of RNA viruses, including Sendai virus (SeV), Vesicular stomatitis virus, Newcastle disease virus, Sindbis virus, and Hepatitis C virus (HCV) is suppressed by type I interferon (IFN) (IFN-a and IFN-b) produced rapidly from the cells after infection of viruses [1,2]. After recognition of RNA virus infection by those receptors, signal cascades for induction of IFNs are stimulated and result in the activation of IFN regulatory factor (IRF)-3, and IRF-7 which are transcription factors for induction of type I IFN genes [3,4]. The primary role of type I IFN is to limit spread of a variety of pathogens via initiation of the innate immune responses through induction of the genes encoding cytokines and antiviral proteins during the first days of infection [5]. These proteins exhibit antiviral effects both directly by inhibiting viral replication and indirectly by stimulating the adaptive immune system

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