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Suggested role of the Golgi apparatus and endoplasmic reticulum for crucial sites of hepatitis C virus replication in human lymphoblastoid cells infected in vitro
Author(s) -
Serafino Annalucia,
Valli Maria Beatrice,
Andreola Federica,
Crema Annalisa,
Ravagnan Giampietro,
Bertolini Luisa,
Carloni Guido
Publication year - 2003
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.10367
Subject(s) - endoplasmic reticulum , biology , virology , golgi apparatus , viral replication , virus , intracellular , cell fusion , cell culture , microbiology and biotechnology , genetics
Iacovacci et al. [(1997a) Research in Virology 148:147–151] described that the euploid diploid cells, of the normal human bone marrow‐derived lymphoblastoid B‐cell line TO.FE., are susceptible to hepatitis C virus (HCV) infection and support long term virus production. Transmission electron microscopy described some steps of HCV replication cycle in this in vitro infected cellular system [Serafino et al. (1997) Research in Virology 148:153–159]. In the present study, in order to identify the intracellular sites involved in HCV replication, the ultrastructural changes associated with infection in TO.FE. cells were correlated with the subcellular localisation of structural and nonstructural viral proteins. Transmission electron microscopy and confocal microscopy data indicate that these viral proteins appeared located in the Golgi apparatus and endoplasmic reticulum, suggesting an active involvement of these compartments in viral assembly and morphogenesis. Furthermore, transmission and scanning electron microscopic observations on cultures infected chronically support the hypothesis that these cellular compartments may serve as starting sites of the morphological changes associated to viral infection and replication, leading to cell‐cell fusion, syncytia formation, and finally lysis of infected cells and virus release. J. Med. Virol. 70: 31–41, 2003. © 2003 Wiley‐Liss, Inc.