Pseudotype hepatitis C virus enters immature myeloid dendritic cells through the interaction with lectin》.pdf

Virology 324 (2004) 74–83 /locate/yviro Pseudotype hepatitis C virus enters immature myeloid dendritic cells through the interaction with lectin Aki Kaimori, a Tatsuya Kanto,a,b Chang Kwang Limn,c Yasumasa Komoda, c Chika Oki,a Michiyo Inoue, a,b Hideki Miyatake, a Ichiyo Itose, a Mitsuru Sakakibara, a Takayuki Yakushijin,a Tetsuo Takehara,a Yoshiharu Matsuura, c and Norio Hayashia,* a Department of Molecular Therapeutics, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan b Department of Dendritic Cell Biology and Clinical Application, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan c Research Center for Emerging Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan Received 14 October 2003; returned to author for revision 12 November 2003; accepted 24 March 2004 Abstract Dendritic cells (DC) are the most potent antigen-presenting cells that regulate immune responses. One of the mechanisms for hepatitis C virus (HCV) persistence is the ability of HCV to suppress DC function. Direct HCV infection to blood DC has been implicated for DC dysfunction. To clarify the susceptibility of each DC subset to HCV, we used pseudotype vesicular stomatitis virus (VSV) coated with chimeric HCV envelope glycoproteins (E1 and E2). We demonstrate that pseudotype VSV enters myeloid DC (MDC) but not plasmacytoid DC (PDC). The highest efficiency of pseudotype VSV entry to MDC was observed when MDC were cultured with G