Pseudotype hepatitis C virus enters immature myeloid dendritic cells through the interaction with lectin.
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.
Kaimori
Aki
A
Department of Molecular Therapeutics, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Kanto
Tatsuya
T
Kwang Limn
Chang
C
Komoda
Yasumasa
Y
Oki
Chika
C
Inoue
Michiyo
M
Miyatake
Hideki
H
Itose
Ichiyo
I
Sakakibara
Mitsuru
M
Yakushijin
Takayuki
T
Takehara
Tetsuo
T
Matsuura
Yoshiharu
Y
Hayashi
Norio
N
D002478:Cells, Cultured; D003713:Dendritic Cells / Q000821:virology*; D016174:Hepacivirus / Q000502:physiology*; D006801:Humans; D037102:Lectins / Q000502:physiology*; D022423:Myeloid Cells / Q000821:virology*; D014721:Vesicular stomatitis Indiana virus / Q000235:genetics; D014759:Viral Envelope Proteins / Q000502:physiology*; D015678:Viral Structural Proteins / Q000502:physiology*
D037102:Lectins; D014759:Viral Envelope Proteins; D015678:Viral Structural Proteins; C107842:protein E1, Classical swine fever virus; C091015:glycoprotein E2, Hepatitis C virus