Hepatitis C virus present in the sera of infected patients interferes with the autophagic process of monocytes impairing their in-vitro differentiation into dendritic cells

Marisa Granato, Valentina Lacconi, Marina Peddis, Livia Di Renzo, Sandro Valia, Daniela Rivanera, Guido Antonelli, Luigi Frati, Alberto Faggioni, Mara Cirone

Research output: Contribution to journalArticle


Autophagy has a pivotal role in the in-vitro monocyte differentiation into macrophages and dendritic cells (DCs), the most powerful antigen presenting cells (APC) with the unique capacity to initiate an adaptive immune response. Autophagy is also a mechanism by which these cells of innate immunity may degrade intracellular pathogens and mediate the antigen processing and presentation, essential to clear an infection. For these reasons, pathogens have learned how to manipulate autophagy for their own survival. In this study we found that hepatitis C virus (HCV), derived from sera of infected patients, blocked the autophagic process in differentiating monocytes, seen as LC3 II and p62 expression levels. The suppression of autophagy correlated with a reduction of cathepsins D, B and proteolytic activity, and resulted in impairment of monocyte differentiation into DCs, as indicated by the reduction of CD1a acquirement. These data suggest that the block of autophagy might be one of the underlying mechanisms of the HCV-mediated immune subversion that frequently leads to viral persistence and chronic hepatitis.

Original languageEnglish
Pages (from-to)1348-1355
Number of pages8
JournalBiochimica et Biophysica Acta - Molecular Cell Research
Issue number7
Publication statusPublished - 2014



  • Autophagy
  • Cathepsin B
  • Cathepsin D
  • Dendritic cells
  • HCV

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Medicine(all)

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