Mosquito cells bind and replicate hepatitis C virus
✍ Scribed by Raphaële Germi; Jean-Marc Crance; Daniel Garin; Josette Guimet; Marie-Ange Thelu; Alain Jouan; Jean-Pierre Zarski; Emmanuel Drouet
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 150 KB
- Volume
- 64
- Category
- Article
- ISSN
- 0146-6615
- DOI
- 10.1002/jmv.1010
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Several studies have demonstrated some hepatitis C virus (HCV) replication in lymphocyte and hepatocyte cell lines such as in African green monkey Vero cells. The aim of the present study was to select other cell lines able to bind and replicate HCV. Human hepatoma PLC/PRF/5 cells, human lymphoma Namalwa cells, Vero and mosquito AP61 cells were inoculated with HCV‐positive plasma, washed six times and examined for the presence of the viral genome at different times post infection, using an RT‐PCR method. Binding of HCV to cells was estimated by HCV RNA detection in cells 2 hr after inoculation and in the last wash of these cells. Successive virus passages in cells were carried out. All the cells studied were able to bind HCV but only AP61 and Vero cells provided evidence of replication and production of infectious virus: virus RNA was detected during 28 days post‐infection in four successive virus passages. CD81 molecules, a putative HCV receptor, were detected by cytofluorometric analysis. Vero cells express CD81 molecules whereas these molecules were not detected on AP61 cells. It is suggested that other receptors are involved in HCV binding to Vero and AP61 cells. J. Med. Virol. 64:6–12, 2001. © 2001 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES
We assessed the correlation between hepatitis C virus replication and antibody responses toward hepatitis C virus core ((222-31, NS3 (C33C1, NS4 (5-1-1 and C100-3) and NS5 proteins in 59 virus carriers. The concentration of serum hepatitis C virus RNA was determined by a competitive reverse transcri
Initiation of hepatitis C virus (HCV) infection is mediated by docking of the viral envelope to the hepatocyte cell surface membrane followed by entry of the virus into the host cell. Aiming to elucidate the impact of this interaction on host cell biology, we performed a genomic analysis of the host
CD56 ؉ T cells are abundant in liver and play an important role in defense against viral infections. However, the role of CD56 ؉ T cells in control of hepatitis C virus (HCV) infection remains to be determined. We investigated the noncytolytic anti-HCV activity of primary CD56 ؉ T cells in human hep