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Interplay among cellular polarization, lipoprotein metabolism and hepatitis C virus entry
Ignacio Benedicto, Francisca Molina-Jiménez, Manuel López-Cabrera, Pedro L Majano, Molecular Biology Unit, Hospital Universitario de la Princesa, Instituto de Investigación Sanitaria Princesa (IP), Madrid 28006, Spain
Ignacio Benedicto, Ricardo Moreno-Otero, Manuel López-Cabrera, Pedro L Majano, CIBERehd, Instituto de Salud Carlos III, Madrid 28029, Spain
Ricardo Moreno-Otero, Liver Unit, Hospital Universitario de la Princesa, Instituto de Investigación Sanitaria Princesa (IP), Madrid 28006, Spain
Manuel López-Cabrera, Centro de Biología Molecular Severo Ochoa, CSIC-UAM, Madrid 28049, Spain
Author contributions: Benedicto I and Majano PL conceived, designed, and wrote the manuscript; Molina-Jiménez F, Moreno-Otero R and López-Cabrera M contributed to the design and critical revision of the article.
Supported by CIBERehd to Moreno-Otero R, López-Cabrera M and Majano PL; SAF2007-61201 (Ministerio de Educación y Ciencia) to López-Cabrera M; CP03/0020 (Instituto de Salud Carlos III), SAF2007-60677 (Ministerio de Educación y Ciencia) and PI10/00101 (Ministerio de Ciencia e Innovación, Instituto de Salud Carlos III, FEDER) to Majano PL. Benedicto I was financially supported by CIBERehd and Molina-Jiménez F by Instituto de Salud Carlos III and FIB Hospital de la Princesa
Correspondence to: Dr. Pedro L Majano, Molecular Biology Unit, Hospital Universitario de la Princesa, C/Diego de León 62, 28006 Madrid, Spain. email@example.com
Telephone: +34-91-5202334 Fax: +34-91-3093911
Received: October 21, 2010
Revised: December 23, 2010
Accepted: December 30, 2010
Published online: June 14, 2011
Hepatitis C virus (HCV) infects more than three million new individuals worldwide each year. In a high percentage of patients, acute infections become chronic, eventually progressing to fibrosis, cirrhosis, and hepatocellular carcinoma. Given the lack of effective prophylactic or therapeutic vaccines, and the limited sustained virological response rates to current therapies, new approaches are needed to prevent, control, and clear HCV infection. Entry into the host cell, being the first step of the viral cycle, is a potential target for the design of new antiviral compounds. Despite the recent discovery of the tight junction-associated proteins claudin-1 and occludin as HCV co-receptors, which is an important step towards the understanding of HCV entry, the precise mechanisms are still largely unknown. In addition, increasing evidence indicates that tools that are broadly employed to study HCV infection do not accurately reflect the real process in terms of viral particle composition and host cell phenotype. Thus, systems that more closely mimic natural infection are urgently required to elucidate the mechanisms of HCV entry, which will in turn help to design antiviral strategies against this part of the infection process.