P
Pablo Gastaminza
Researcher at Spanish National Research Council
Publications - 53
Citations - 5568
Pablo Gastaminza is an academic researcher from Spanish National Research Council. The author has contributed to research in topics: Hepatitis C virus & Viral replication. The author has an hindex of 22, co-authored 47 publications receiving 5191 citations. Previous affiliations of Pablo Gastaminza include University of Barcelona & Carlos III Health Institute.
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Journal ArticleDOI
Robust hepatitis C virus infection in vitro
Jin Zhong,Pablo Gastaminza,Guofeng Cheng,Sharookh B. Kapadia,Takanobu Kato,Dennis R. Burton,Stefan Wieland,Susan L. Uprichard,Takaji Wakita,Francis V. Chisari +9 more
TL;DR: A simple yet robust HCV cell culture infection system based on the HCV JFH-1 molecular clone and Huh-7-derived cell lines that allows the production of virus that can be efficiently propagated in tissue culture is reported.
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Broadly neutralizing antibodies protect against hepatitis C virus quasispecies challenge
Mansun Law,Toshiaki Maruyama,Jamie T. Lewis,Erick Giang,Alexander W. Tarr,Zania Stamataki,Pablo Gastaminza,Francis V. Chisari,Ian M. Jones,Robert I. Fox,Jonathan K. Ball,Jane A. McKeating,Norman M. Kneteman,Dennis R. Burton +13 more
TL;DR: The results provide evidence that broadly neutralizing antibodies to HCV protect against heterologous viral infection and suggest that a prophylactic vaccine against HCV may be achievable.
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Cellular Determinants of Hepatitis C Virus Assembly, Maturation, Degradation, and Secretion
TL;DR: The results suggest that by coopting the VLDL assembly, maturation, degradation, and secretory machinery of the cell, HCV acquires its hepatocyte tropism and, by mimicry, its tendency to persist.
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The autophagy machinery is required to initiate hepatitis C virus replication
TL;DR: Autophagy proteins are proviral factors required for translation of incoming hepatitis C virus (HCV) RNA and, thereby, for initiation of HCV replication, but they are not required once infection is established, suggesting that different host factors regulate thetranslation of incoming viral genome and translation of progeny HCV RNA once replication is established.
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Plasmacytoid dendritic cells sense hepatitis C virus–infected cells, produce interferon, and inhibit infection
Ken Takahashi,Shinichi Asabe,Stefan Wieland,Urtzi Garaigorta,Pablo Gastaminza,Masanori Isogawa,Francis V. Chisari +6 more
TL;DR: It is reported that HCV-infected cells trigger a robust IFN response in plasmacytoid dendritic cells (pDCs) by a mechanism that requires active viral replication, direct cell-cell contact, and Toll-like receptor 7 signaling, and it is shown that the activated pDC supernatant inhibits HCV infection in an IFN receptor-dependent manner.