Measles virus circumvents the host interferon response by different actions of the C and V proteins

Yuichiro Nakatsu, Makoto Takeda, Shinji Ohno, Yuta Shirogane, Masaharu Iwasaki, Yusuke Yanagi

研究成果: ジャーナルへの寄稿記事

76 引用 (Scopus)

抄録

Measles is an acute febrile infectious disease with high morbidity and mortality. The genome of measles virus (MV), the causative agent, encodes two accessory products, V and C proteins, that play important roles in MV virulence. The V but not the C protein of the IC-B strain (a well-characterized virulent strain of MV) has been shown to block the Jak/Stat signaling pathway and counteract the cellular interferon (IFN) response. We have recently shown that a recombinant IC-B strain that lacks C protein expression replicates poorly in certain cell lines, and its growth defect is related to translational inhibition and strong IFN induction. Here, we show that the V protein of the MV IC-B strain also blocks the IFN induction pathway mediated by the melanoma differentiation-associated gene 5 product, thus actively interfering with the host IFN response at two different steps. On the other hand, the C protein per se possesses no activity to block the IFN induction pathway. Our data indicate that the C protein acts as a regulator of viral RNA synthesis, thereby acting indirectly to suppress IFN induction. Since recombinant MVs with C protein defective in modulating viral RNA synthesis or lacking C protein expression strongly stimulate IFN production, in spite of V protein production, both the C and V proteins must be required for MV to fully circumvent the host IFN response.

元の言語英語
ページ(範囲)8296-8306
ページ数11
ジャーナルJournal of virology
82
発行部数17
DOI
出版物ステータス出版済み - 9 1 2008

Fingerprint

Measles virus
interferons
Protein C
Interferons
proteins
Viral RNA
protein synthesis
RNA
synthesis
Measles
melanoma
infectious diseases
fever
Communicable Diseases
morbidity
Virulence
Melanoma
Fever
virulence
cell lines

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

これを引用

Measles virus circumvents the host interferon response by different actions of the C and V proteins. / Nakatsu, Yuichiro; Takeda, Makoto; Ohno, Shinji; Shirogane, Yuta; Iwasaki, Masaharu; Yanagi, Yusuke.

:: Journal of virology, 巻 82, 番号 17, 01.09.2008, p. 8296-8306.

研究成果: ジャーナルへの寄稿記事

Nakatsu, Yuichiro ; Takeda, Makoto ; Ohno, Shinji ; Shirogane, Yuta ; Iwasaki, Masaharu ; Yanagi, Yusuke. / Measles virus circumvents the host interferon response by different actions of the C and V proteins. :: Journal of virology. 2008 ; 巻 82, 番号 17. pp. 8296-8306.
@article{a7c1baad871649c3b51aaa7f647d4e54,
title = "Measles virus circumvents the host interferon response by different actions of the C and V proteins",
abstract = "Measles is an acute febrile infectious disease with high morbidity and mortality. The genome of measles virus (MV), the causative agent, encodes two accessory products, V and C proteins, that play important roles in MV virulence. The V but not the C protein of the IC-B strain (a well-characterized virulent strain of MV) has been shown to block the Jak/Stat signaling pathway and counteract the cellular interferon (IFN) response. We have recently shown that a recombinant IC-B strain that lacks C protein expression replicates poorly in certain cell lines, and its growth defect is related to translational inhibition and strong IFN induction. Here, we show that the V protein of the MV IC-B strain also blocks the IFN induction pathway mediated by the melanoma differentiation-associated gene 5 product, thus actively interfering with the host IFN response at two different steps. On the other hand, the C protein per se possesses no activity to block the IFN induction pathway. Our data indicate that the C protein acts as a regulator of viral RNA synthesis, thereby acting indirectly to suppress IFN induction. Since recombinant MVs with C protein defective in modulating viral RNA synthesis or lacking C protein expression strongly stimulate IFN production, in spite of V protein production, both the C and V proteins must be required for MV to fully circumvent the host IFN response.",
author = "Yuichiro Nakatsu and Makoto Takeda and Shinji Ohno and Yuta Shirogane and Masaharu Iwasaki and Yusuke Yanagi",
year = "2008",
month = "9",
day = "1",
doi = "10.1128/JVI.00108-08",
language = "English",
volume = "82",
pages = "8296--8306",
journal = "Journal of Virology",
issn = "0022-538X",
publisher = "American Society for Microbiology",
number = "17",

}

TY - JOUR

T1 - Measles virus circumvents the host interferon response by different actions of the C and V proteins

AU - Nakatsu, Yuichiro

AU - Takeda, Makoto

AU - Ohno, Shinji

AU - Shirogane, Yuta

AU - Iwasaki, Masaharu

AU - Yanagi, Yusuke

PY - 2008/9/1

Y1 - 2008/9/1

N2 - Measles is an acute febrile infectious disease with high morbidity and mortality. The genome of measles virus (MV), the causative agent, encodes two accessory products, V and C proteins, that play important roles in MV virulence. The V but not the C protein of the IC-B strain (a well-characterized virulent strain of MV) has been shown to block the Jak/Stat signaling pathway and counteract the cellular interferon (IFN) response. We have recently shown that a recombinant IC-B strain that lacks C protein expression replicates poorly in certain cell lines, and its growth defect is related to translational inhibition and strong IFN induction. Here, we show that the V protein of the MV IC-B strain also blocks the IFN induction pathway mediated by the melanoma differentiation-associated gene 5 product, thus actively interfering with the host IFN response at two different steps. On the other hand, the C protein per se possesses no activity to block the IFN induction pathway. Our data indicate that the C protein acts as a regulator of viral RNA synthesis, thereby acting indirectly to suppress IFN induction. Since recombinant MVs with C protein defective in modulating viral RNA synthesis or lacking C protein expression strongly stimulate IFN production, in spite of V protein production, both the C and V proteins must be required for MV to fully circumvent the host IFN response.

AB - Measles is an acute febrile infectious disease with high morbidity and mortality. The genome of measles virus (MV), the causative agent, encodes two accessory products, V and C proteins, that play important roles in MV virulence. The V but not the C protein of the IC-B strain (a well-characterized virulent strain of MV) has been shown to block the Jak/Stat signaling pathway and counteract the cellular interferon (IFN) response. We have recently shown that a recombinant IC-B strain that lacks C protein expression replicates poorly in certain cell lines, and its growth defect is related to translational inhibition and strong IFN induction. Here, we show that the V protein of the MV IC-B strain also blocks the IFN induction pathway mediated by the melanoma differentiation-associated gene 5 product, thus actively interfering with the host IFN response at two different steps. On the other hand, the C protein per se possesses no activity to block the IFN induction pathway. Our data indicate that the C protein acts as a regulator of viral RNA synthesis, thereby acting indirectly to suppress IFN induction. Since recombinant MVs with C protein defective in modulating viral RNA synthesis or lacking C protein expression strongly stimulate IFN production, in spite of V protein production, both the C and V proteins must be required for MV to fully circumvent the host IFN response.

UR - http://www.scopus.com/inward/record.url?scp=50149115159&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=50149115159&partnerID=8YFLogxK

U2 - 10.1128/JVI.00108-08

DO - 10.1128/JVI.00108-08

M3 - Article

C2 - 18562542

AN - SCOPUS:50149115159

VL - 82

SP - 8296

EP - 8306

JO - Journal of Virology

JF - Journal of Virology

SN - 0022-538X

IS - 17

ER -