Pseudotype hepatitis C virus enters immature myeloid dendritic cells through the interaction with lectin - PubMed (original) (raw)

. 2004 Jun 20;324(1):74-83.

doi: 10.1016/j.virol.2004.03.038.

Tatsuya Kanto, Chang Kwang Limn, Yasumasa Komoda, Chika Oki, Michiyo Inoue, Hideki Miyatake, Ichiyo Itose, Mitsuru Sakakibara, Takayuki Yakushijin, Tetsuo Takehara, Yoshiharu Matsuura, Norio Hayashi

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

Aki Kaimori et al. Virology. 2004.

Free article

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 GM-CSF. Such efficiency decreased when MDC are matured with the treatment of IL-4, CpG oligodeoxynucleotide, or CD40 ligand. Mannan inhibited pseudotype VSV entry to MDC, but Ca(2+) chelators failed to do so. These results show that pseudotype VSV possessing HCV-E1 and E2 enters immature MDC through the interaction with lectins in a Ca(2+)-independent manner.

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