A polymorphism of the TIM-1 IgV domain

Implications for the susceptibility to filovirus infection

Makoto Kuroda, Daisuke Fujikura, Osamu Noyori, Masahiro Kajihara, Junki Maruyama, Hiroko Miyamoto, Reiko Yoshida, Ayato Takada

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Filoviruses, including Ebola and Marburg viruses, cause severe hemorrhagic fever in humans and nonhuman primates with mortality rates of up to 90%. Human T-cell immunoglobulin and mucin domain 1 (TIM-1) is one of the host proteins that have been shown to promote filovirus entry into cells. In this study, we cloned TIM-1 genes from three different African green monkey kidney cell lines (Vero E6, COS-1, and BSC-1) and found that TIM-1 of Vero E6 had a 23-amino acid deletion and 6 amino acid substitutions compared with those of COS-1 and BSC-1. Interestingly, Vero E6 TIM-1 had a greater ability to promote the infectivity of vesicular stomatitis viruses pseudotyped with filovirus glycoproteins than COS-1-derived TIM-1. We further found that the increased ability of Vero E6 TIM-1 to promote virus infectivity was most likely due to a single amino acid difference between these TIM-1s. These results suggest that a polymorphism of the TIM-1 molecules is one of the factors that influence cell susceptibility to filovirus infection, providing a new insight into the molecular basis for the filovirus host range.

Original languageEnglish (US)
Pages (from-to)223-228
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume455
Issue number3-4
DOIs
StatePublished - Dec 12 2014
Externally publishedYes

Fingerprint

Polymorphism
Viruses
Marburgvirus
Ebolavirus
Amino Acids
Cercopithecus aethiops
Mucin-1
Vesicular Stomatitis
Host Specificity
Amino Acid Substitution
Infection
Primates
Glycoproteins
Fever
T-cells
Mucins
T-Lymphocytes
Kidney
Cell Line
Mortality

Keywords

  • Entry
  • Filovirus
  • Polymorphism
  • Receptor
  • Susceptibility
  • TIM-1

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Molecular Biology
  • Medicine(all)

Cite this

A polymorphism of the TIM-1 IgV domain : Implications for the susceptibility to filovirus infection. / Kuroda, Makoto; Fujikura, Daisuke; Noyori, Osamu; Kajihara, Masahiro; Maruyama, Junki; Miyamoto, Hiroko; Yoshida, Reiko; Takada, Ayato.

In: Biochemical and Biophysical Research Communications, Vol. 455, No. 3-4, 12.12.2014, p. 223-228.

Research output: Contribution to journalArticle

Kuroda, Makoto ; Fujikura, Daisuke ; Noyori, Osamu ; Kajihara, Masahiro ; Maruyama, Junki ; Miyamoto, Hiroko ; Yoshida, Reiko ; Takada, Ayato. / A polymorphism of the TIM-1 IgV domain : Implications for the susceptibility to filovirus infection. In: Biochemical and Biophysical Research Communications. 2014 ; Vol. 455, No. 3-4. pp. 223-228.
@article{6dc6cd50772542c79defaa79956fb791,
title = "A polymorphism of the TIM-1 IgV domain: Implications for the susceptibility to filovirus infection",
abstract = "Filoviruses, including Ebola and Marburg viruses, cause severe hemorrhagic fever in humans and nonhuman primates with mortality rates of up to 90{\%}. Human T-cell immunoglobulin and mucin domain 1 (TIM-1) is one of the host proteins that have been shown to promote filovirus entry into cells. In this study, we cloned TIM-1 genes from three different African green monkey kidney cell lines (Vero E6, COS-1, and BSC-1) and found that TIM-1 of Vero E6 had a 23-amino acid deletion and 6 amino acid substitutions compared with those of COS-1 and BSC-1. Interestingly, Vero E6 TIM-1 had a greater ability to promote the infectivity of vesicular stomatitis viruses pseudotyped with filovirus glycoproteins than COS-1-derived TIM-1. We further found that the increased ability of Vero E6 TIM-1 to promote virus infectivity was most likely due to a single amino acid difference between these TIM-1s. These results suggest that a polymorphism of the TIM-1 molecules is one of the factors that influence cell susceptibility to filovirus infection, providing a new insight into the molecular basis for the filovirus host range.",
keywords = "Entry, Filovirus, Polymorphism, Receptor, Susceptibility, TIM-1",
author = "Makoto Kuroda and Daisuke Fujikura and Osamu Noyori and Masahiro Kajihara and Junki Maruyama and Hiroko Miyamoto and Reiko Yoshida and Ayato Takada",
year = "2014",
month = "12",
day = "12",
doi = "10.1016/j.bbrc.2014.10.144",
language = "English (US)",
volume = "455",
pages = "223--228",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "3-4",

}

TY - JOUR

T1 - A polymorphism of the TIM-1 IgV domain

T2 - Implications for the susceptibility to filovirus infection

AU - Kuroda, Makoto

AU - Fujikura, Daisuke

AU - Noyori, Osamu

AU - Kajihara, Masahiro

AU - Maruyama, Junki

AU - Miyamoto, Hiroko

AU - Yoshida, Reiko

AU - Takada, Ayato

PY - 2014/12/12

Y1 - 2014/12/12

N2 - Filoviruses, including Ebola and Marburg viruses, cause severe hemorrhagic fever in humans and nonhuman primates with mortality rates of up to 90%. Human T-cell immunoglobulin and mucin domain 1 (TIM-1) is one of the host proteins that have been shown to promote filovirus entry into cells. In this study, we cloned TIM-1 genes from three different African green monkey kidney cell lines (Vero E6, COS-1, and BSC-1) and found that TIM-1 of Vero E6 had a 23-amino acid deletion and 6 amino acid substitutions compared with those of COS-1 and BSC-1. Interestingly, Vero E6 TIM-1 had a greater ability to promote the infectivity of vesicular stomatitis viruses pseudotyped with filovirus glycoproteins than COS-1-derived TIM-1. We further found that the increased ability of Vero E6 TIM-1 to promote virus infectivity was most likely due to a single amino acid difference between these TIM-1s. These results suggest that a polymorphism of the TIM-1 molecules is one of the factors that influence cell susceptibility to filovirus infection, providing a new insight into the molecular basis for the filovirus host range.

AB - Filoviruses, including Ebola and Marburg viruses, cause severe hemorrhagic fever in humans and nonhuman primates with mortality rates of up to 90%. Human T-cell immunoglobulin and mucin domain 1 (TIM-1) is one of the host proteins that have been shown to promote filovirus entry into cells. In this study, we cloned TIM-1 genes from three different African green monkey kidney cell lines (Vero E6, COS-1, and BSC-1) and found that TIM-1 of Vero E6 had a 23-amino acid deletion and 6 amino acid substitutions compared with those of COS-1 and BSC-1. Interestingly, Vero E6 TIM-1 had a greater ability to promote the infectivity of vesicular stomatitis viruses pseudotyped with filovirus glycoproteins than COS-1-derived TIM-1. We further found that the increased ability of Vero E6 TIM-1 to promote virus infectivity was most likely due to a single amino acid difference between these TIM-1s. These results suggest that a polymorphism of the TIM-1 molecules is one of the factors that influence cell susceptibility to filovirus infection, providing a new insight into the molecular basis for the filovirus host range.

KW - Entry

KW - Filovirus

KW - Polymorphism

KW - Receptor

KW - Susceptibility

KW - TIM-1

UR - http://www.scopus.com/inward/record.url?scp=84914180828&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84914180828&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2014.10.144

DO - 10.1016/j.bbrc.2014.10.144

M3 - Article

VL - 455

SP - 223

EP - 228

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 3-4

ER -