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4. TRIM25 Enhances the Antiviral Action of Zinc-Finger Antiviral Protein (ZAP).

Author

Li, Melody MH, Lau, Zerlina, Cheung, Pamela, Aguilar, Eduardo G, Schneider, William M, Bozzacco, Leonia, Molina, Henrik, Buehler, Eugen, Takaoka, Akinori, Rice, Charles M, Felsenfeld, Dan P, and MacDonald, Margaret R

Subjects
Cell Line, Animals, Humans, Sindbis Virus, Alphavirus Infections, Ubiquitin-Protein Ligases, RNA-Binding Proteins, Interferon Type I, Protein Isoforms, Transcription Factors, RNA, Small Interfering, Antiviral Agents, RNA Interference, Cricetinae, Ubiquitination, HEK293 Cells, Tripartite Motif Proteins, Protein Domains, RNA, Small Interfering, Virology, Microbiology, Immunology, Medical Microbiology
Abstract

The host factor and interferon (IFN)-stimulated gene (ISG) product, zinc-finger antiviral protein (ZAP), inhibits a number of diverse viruses by usurping and intersecting with multiple cellular pathways. To elucidate its antiviral mechanism, we perform a loss-of-function genome-wide RNAi screen to identify cellular cofactors required for ZAP antiviral activity against the prototype alphavirus, Sindbis virus (SINV). In order to exclude off-target effects, we carry out stringent confirmatory assays to verify the top hits. Important ZAP-liaising partners identified include proteins involved in membrane ion permeability, type I IFN signaling, and post-translational protein modification. The factor contributing most to the antiviral function of ZAP is TRIM25, an E3 ubiquitin and ISG15 ligase. We demonstrate here that TRIM25 interacts with ZAP through the SPRY domain, and TRIM25 mutants lacking the RING or coiled coil domain fail to stimulate ZAP's antiviral activity, suggesting that both TRIM25 ligase activity and its ability to form oligomers are critical for its cofactor function. TRIM25 increases the modification of both the short and long ZAP isoforms by K48- and K63-linked polyubiquitin, although ubiquitination of ZAP does not directly affect its antiviral activity. However, TRIM25 is critical for ZAP's ability to inhibit translation of the incoming SINV genome. Taken together, these data uncover TRIM25 as a bona fide ZAP cofactor that leads to increased ZAP modification enhancing its translational inhibition activity.

Published
2017

11. Contributors

Author

Amano, Masafumi, primary, Ando, Hironori, additional, Andoh, Tadashi, additional, Baker, Michael E., additional, Cameron, Melissa S., additional, Daubnerová, Ivana, additional, Donald, John A., additional, Fukumura, Keisuke, additional, Funaba, Masayuki, additional, Haraguchi, Shogo, additional, Hayakawa, Yoichi, additional, Hirako, Satoshi, additional, Hyodo, Susumu, additional, Iguchi, Taisen, additional, Inui, Akio, additional, Kaiya, Hiroyuki, additional, Kakizawa, Sho, additional, Kamiyama, Takumi, additional, Kanamori, Yohei, additional, Kanda, Shinji, additional, Katayama, Hidekazu, additional, Kato, Takashi, additional, Katsu, Yoshinao, additional, Katsuura, Goro, additional, Kawada, Tsuyoshi, additional, Kimura, Atsushi P., additional, Kitamura, Keiichiro, additional, Kobayashi, Yuki, additional, Kodani, Yu, additional, Konno, Norifumi, additional, Kuraku, Shigehiro, additional, Minakata, Hiroyuki, additional, Mita, Masatoshi, additional, Miyagawa, Shinichi, additional, Miyazato, Mikiya, additional, Mizusawa, Kanta, additional, Mori, Kenji, additional, Morishita, Fumihiro, additional, Moriyama, Shunsuke, additional, Nagasaki, Hiroshi, additional, Nagata, Shinji, additional, Nakamachi, Tomoya, additional, Niwa, Ryusuke, additional, Ogino, Yukiko, additional, Ogoshi, Maho, additional, Ohira, Tsuyoshi, additional, Ohki-Hamazaki, Hiroko, additional, Ohtaki, Hirokazu, additional, Ohyama, Yoshihiko, additional, Oka, Yoshitaka, additional, Okamoto, Naoki, additional, Onizawa, Moe, additional, Osugi, Tomohiro, additional, Saito, Yumiko, additional, Sakai, Takafumi, additional, Sakamoto, Hirotaka, additional, Sakamoto, Tatsuya, additional, Sakata, Ichiro, additional, Satake, Honoo, additional, Sato, Seiichi, additional, Sato, Tomomi, additional, Seike, Hitomi, additional, Sekiguchi, Toshio, additional, Shimizu, Munetaka, additional, Shinki, Toshimasa, additional, Shinoda, Tetsuro, additional, Shiomi, Kunihiro, additional, Suzuki, Nobuo, additional, Tachibana, Tetsuya, additional, Takahashi, Akiyoshi, additional, Takahashi, Toshio, additional, Takaoka, Akinori, additional, Takei, Yoshio, additional, Takenoya, Fumiko, additional, Takeuchi, Sakae, additional, Tanaka, Yoshiaki, additional, Toshinai, Koji, additional, Tsukada, Takehiro, additional, Tsutsui, Kazuyoshi, additional, Tsutsui, Naoaki, additional, Ubuka, Takayoshi, additional, Ukena, Kazuyoshi, additional, Wada, Nobuhiro, additional, Watanabe, Jun, additional, Wong, Marty Kwok-Shing, additional, Yamada, Taisho, additional, Yamaguchi, Yoko, additional, Yamanaka, Naoki, additional, Yamauchi, Kiyoshi, additional, Yuge, Shinya, additional, Zhou, Yijun, additional, and Žitňan, Dušan, additional

Published
2021
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14. Integrin α9 on lymphatic endothelial cells regulates lymphocyte egress.

Author

Ito, Koyu, Morimoto, Junko, Kihara, Akio, Matsui, Yutaka, Kurotaki, Daisuke, Kanayama, Masashi, Simmons, Szandor, Ishii, Masaru, Takaoka, Akinori, Uede, Toshimitsu, and Sheppard, Dean

Subjects
autoimmune disease, lymphocyte trafficking, matricellular proteins, Animals, Encephalomyelitis, Autoimmune, Experimental, Endothelial Cells, Flow Cytometry, Freunds Adjuvant, Histological Techniques, Immunologic Surveillance, Integrin alpha Chains, Lymph Nodes, Lymphocytes, Lysophospholipids, Mice, Mice, Inbred C57BL, Microscopy, Confocal, Sphingosine, Statistics, Nonparametric, Tenascin
Abstract

Sphingosine 1-phosphate (S1P) plays a role in lymphocyte egress from lymphoid organs. However, it remains unclear how S1P production and secretion are regulated. We show that under inflammatory conditions, α9 integrin, which is closely associated with activated β1 integrin, and its ligand, tenascin-C, colocalize on medullary and cortical sinuses of draining lymph nodes (dLNs), which is a gate for lymphocyte exit, and that inhibition of lymphocyte egress is evident by blockade of α9 integrin-mediated signaling at dLNs. Based on in vitro analysis using lymphatic endothelial cells obtained from mice embryos, we suggested the possibility that stimulation of lymphatic endothelial cells by tenascin-C enhances S1P secretion in an α9 integrin-dependent manner without affecting S1P synthesis and/or degradation. Blockade of α9 integrin-mediated signaling reduced lymphocyte egress from dLNs in several models, including experimental autoimmune encephalomyelitis, where it improved clinical scores and pathology. Therefore, manipulating α9 integrin function may offer a therapeutic strategy for treating various inflammatory disorders.

Published
2014

21. Augmented interferon regulatory factor 7 axis in whole tumor cell vaccines prevents tumor recurrence by inducing interferon gamma-secreting B cells

Author

Kajihara, Nabeel, primary, Tanaka, Yoshino, additional, Takeuchi, Riko, additional, Kobayashi, Takuto, additional, Tanji, Masafumi, additional, Ataka, Tsukasa, additional, Nakano, Shiho, additional, Yamada, Taisho, additional, Takaoka, Akinori, additional, Hasegawa, Yoshinori, additional, Seino, Ken-Ichiro, additional, and Wada, Haruka, additional

Published
2023
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24. Superoxide Dismutase 1 Protects Hepatocytes from Type I Interferon-Driven Oxidative Damage

Author

Bhattacharya, Anannya, Hegazy, Ahmed N., Deigendesch, Nikolaus, Kosack, Lindsay, Cupovic, Jovana, Kandasamy, Richard K., Hildebrandt, Andrea, Merkler, Doron, Kühl, Anja A., Vilagos, Bojan, Schliehe, Christopher, Panse, Isabel, Khamina, Kseniya, Baazim, Hatoon, Arnold, Isabelle, Flatz, Lukas, Xu, Haifeng C., Lang, Philipp A., Aderem, Alan, Takaoka, Akinori, Superti-Furga, Giulio, Colinge, Jacques, Ludewig, Burkhard, Löhning, Max, and Bergthaler, Andreas

Published
2015
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27. Novel Rapid Method for Identifying and Quantifying Pathogenic Bacteria within Four Hours of Blood Collection

Author

Miyakoshi, Akio, primary, Niimi, Hideki, additional, Ueno, Tomohiro, additional, Wakasugi, Masahiro, additional, Higashi, Yoshitsugu, additional, Miyajima, Yuki, additional, Mori, Masashi, additional, Tabata, Homare, additional, Minami, Hiroshi, additional, Takaoka, Akinori, additional, Hayashi, Atsushi, additional, Yamamoto, Yoshihiro, additional, and Kitajima, Isao, additional

Published
2022
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28. Disinfectant potential in inactivation of epidemic keratoconjunctivitis-related adenoviruses by potassium peroxymonosulfate

Author

Hashizume, Mei, Aoki, Koki, Ohno, Shigeaki, Kitaichi, Nobuyoshi, Yawata, Nobuyo, Gonzalez, Gabriel, Nonaka, Hirotaka, Sato, Seiichi, and Takaoka, Akinori

Subjects
Virkon, prevention, RUBYSTA, Human adenovirus, epidemic keratoconjunctivitis, disinfectants
Abstract

Purpose: The aim of this study was to test the antiviral effectivity of potassium peroxymonosulfate (RUBYSTA (R), KYORIN) against five epidemic keratoconjunctivitis-related types of Human adenovirus D in vitro. Methods: Five types of Human adenovirus D (8, 37, 53, 54 and 56) were incubated with 1% potassium peroxymonosulfate, 0.1% sodium hypochlorite (NaClO) or alcohol-based disinfectant for 30 s or 1 min. These solutions were subjected to measurements of viral titres by infection assays in A549 cells. At day 6 post-infection, both, supernatants and cells, were collected and the viral genome was assessed by real-time polymerase chain reaction analysis. Results: Treatments with 1% potassium peroxymonosulfate led to significant reduction in all tested Human adenovirus D types comparable to disinfecting effects by 0.1% NaClO. Overall, potassium peroxymonosulfate demonstrated sufficient inactivation of the major epidemic keratoconjunctivitis-causing Human adenovirus D to be considered for disinfection and prevention purposes in ophthalmological clinics and hospitals. Conclusion: This study demonstrated that potassium peroxymonosulfate is a promising disinfectant for the prevention of epidemic keratoconjunctivitis nosocomial infections in ophthalmological clinics.

Published
2021

39. Dual Effect of Organogermanium Compound THGP on RIG-I-Mediated Viral Sensing and Viral Replication during Influenza a Virus Infection

Author

Baidya, Sunanda, primary, Nishimoto, Yoko, additional, Sato, Seiichi, additional, Shimada, Yasuhiro, additional, Sakurai, Nozomi, additional, Nonaka, Hirotaka, additional, Noguchi, Koki, additional, Kido, Mizuki, additional, Tadano, Satoshi, additional, Ishikawa, Kozo, additional, Li, Kai, additional, Okubo, Aoi, additional, Yamada, Taisho, additional, Orba, Yasuko, additional, Sasaki, Michihito, additional, Sawa, Hirofumi, additional, Miyamoto, Hiroko, additional, Takada, Ayato, additional, Nakamura, Takashi, additional, and Takaoka, Akinori, additional

Published
2021
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40. Dual Effect of Organogermanium Compound THGP on RIG-I-Mediated Viral Sensing and Viral Replication during Influenza a Virus Infection

Author

Baidya, Sunanda, Nishimoto, Yoko, Sato, Seiichi, Shimada, Yasuhiro, Sakurai, Nozomi, Nonaka, Hirotaka, Noguchi, Koki, Kido, Mizuki, Tadano, Satoshi, Ishikawa, Kozo, Li, Kai, Okubo, Aoi, Yamada, Taisho, Orba, Yasuko, Sasaki, Michihito, Sawa, Hirofumi, Miyamoto, Hiroko, Takada, Ayato, Nakamura, Takashi, Takaoka, Akinori, Baidya, Sunanda, Nishimoto, Yoko, Sato, Seiichi, Shimada, Yasuhiro, Sakurai, Nozomi, Nonaka, Hirotaka, Noguchi, Koki, Kido, Mizuki, Tadano, Satoshi, Ishikawa, Kozo, Li, Kai, Okubo, Aoi, Yamada, Taisho, Orba, Yasuko, Sasaki, Michihito, Sawa, Hirofumi, Miyamoto, Hiroko, Takada, Ayato, Nakamura, Takashi, and Takaoka, Akinori

Abstract

The interaction of viral nucleic acid with protein factors is a crucial process for initiating viral polymerase-mediated viral genome replication while activating pattern recognition receptor (PRR)-mediated innate immune responses. It has previously been reported that a hydrolysate of Ge-132, 3-(trihydroxygermyl) propanoic acid (THGP), shows a modulatory effect on microbial infections, inflammation, and immune responses. However, the detailed mechanism by which THGP can modify these processes during viral infections remained unknown. Here, we show that THGP can specifically downregulate type I interferon (IFN) production in response to stimulation with a cytosolic RNA sensor RIG-I ligand 5 '-triphosphate RNA (3pRNA) but not double-stranded RNA, DNA, or lipopolysaccharide. Consistently, treatment with THGP resulted in the dose-dependent suppression of type I IFN induction upon infections with influenza virus (IAV) and vesicular stomatitis virus, which are known to be mainly sensed by RIG-I. Mechanistically, THGP directly binds to the 5 '-triphosphate moiety of viral RNA and competes with RIG-I-mediated recognition. Furthermore, we found that THGP can directly counteract the replication of IAV but not EMCV (encephalitismyocarditis virus), by inhibiting the interaction of viral polymerase with RNA genome. Finally, IAV RNA levels were significantly reduced in the lung tissues of THGP-treated mice when compared with untreated mice. These results suggest a possible therapeutic implication of THGP and show direct antiviral action, together with the suppressive activity of innate inflammation.

Published
2021

41. RIG-I triggers a signaling-abortive anti-SARS-CoV-2 defense in human lung cells

Author

1000010779333, Yamada, Taisho, Sato, Seiichi, Sotoyama, Yuki, Orba, Yasuko, Sawa, Hirofumi, Yamauchi, Hajime, Sasaki, Michihito, 1000030323611, Takaoka, Akinori, 1000010779333, Yamada, Taisho, Sato, Seiichi, Sotoyama, Yuki, Orba, Yasuko, Sawa, Hirofumi, Yamauchi, Hajime, Sasaki, Michihito, 1000030323611, and Takaoka, Akinori

Abstract

Efficient immune responses against viral infection are determined by sufficient activation of nucleic acid sensor-mediated innate immunity(1,2). Coronavirus disease 2019, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains an ongoing global pandemic. It is an urgent challenge to clarify the innate recognition mechanism to control this virus. Here we show that retinoic acid-inducible gene-I (RIG-I) sufficiently restrains SARS-CoV-2 replication in human lung cells in a type I/III interferon (IFN)-independent manner. RIG-I recognizes the 3 ' untranslated region of the SARS-CoV-2 RNA genome via the helicase domains, but not the C-terminal domain. This new mode of RIG-I recognition does not stimulate its ATPase, thereby aborting the activation of the conventional mitochondrial antiviral-signaling protein-dependent pathways, which is in accordance with lack of cytokine induction. Nevertheless, the interaction of RIG-I with the viral genome directly abrogates viral RNA-dependent RNA polymerase mediation of the first step of replication. Consistently, genetic ablation of RIG-I allows lung cells to produce viral particles that expressed the viral spike protein. By contrast, the anti-SARS-CoV-2 activity was restored by all-trans retinoic acid treatment through upregulation of RIG-I protein expression in primary lung cells derived from patients with chronic obstructive pulmonary disease. Thus, our findings demonstrate the distinctive role of RIG-I as a restraining factor in the early phase of SARS-CoV-2 infection in human lung cells.

Published
2021

48. Spatiotemporal regulation of MyD88-IRF-7 signalling for robust type-I interferon induction

Author

Honda, Kenya, Ohba, Yusuke, Yanai, Hideyuki, Negishi, Hideo, Mizutani, Tatsuaki, Takaoka, Akinori, Taya, Choji, and Taniguchi, Tadatsugu

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Kenya Honda [1, 4]; Yusuke Ohba [1, 2, 4]; Hideyuki Yanai [1, 4]; Hideo Negishi [1]; Tatsuaki Mizutani [1]; Akinori Takaoka [1]; Choji Taya [3]; Tadatsugu Taniguchi (corresponding author) [...]

Published
2005
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49. IRF-7 is the master regulator of type-I interferon-dependent immune responses

Author

Honda, Kenya, Yanai, Hideyuki, Negishi, Hideo, Asagiri, Masataka, Sato, Mitsuharu, Mizutani, Tatsuaki, Shimada, Naoya, Ohba, Yusuke, Takaoka, Akinori, Yoshida, Nobuaki, and Taniguchi, Tadatsugu

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Kenya Honda [1, 4]; Hideyuki Yanai [1, 4]; Hideo Negishi [1]; Masataka Asagiri [1]; Mitsuharu Sato [2]; Tatsuaki Mizutani [1]; Naoya Shimada [1]; Yusuke Ohba [1, 3]; Akinori Takaoka [...]

Published
2005
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50. Selective contribution of IFN-[alpha]/[beta] signaling to the maturation of dendritic cells induced by double-stranded RNA or viral infection

Author

Honda, Kenya, Sakaguchi, Shinya, Nakajima, Chigusa, Watanabe, Ai, Yanai, Hideyuki, Matsumoto, Misako, Ohteki, Toshiaki, Kaisho, Tsuneyasu, Takaoka, Akinori, Akira, Shizuo, Seya, Tsukasa, and Taniguchi, Tadatsugu

Subjects
Science and technology
Abstract

A complex mechanism may be operational for dendritic cell (DC) maturation, wherein Toll-like receptor and other signaling pathways may be coordinated differently depending on the nature of the pathogens, in order for DC maturation to be most effective to a given threat. Here, we show that IFN-[alpha]/[beta] signaling is selectively required for the maturation of DCs induced by double-stranded RNA or viral infection in vitro. Interestingly, the maturation is still observed in the absence of either of the two target genes of IFN-[alpha]/[beta], TLR3 and PKR (double-stranded-RNA-dependent protein kinase R), indicating the complexity of the IFN-[alpha]/[beta]-induced transcriptional program in DCs. We also show that the DCs stimulated in vivo by these agents can migrate into the T cell zone of the spleen but fail to mature without the IFN signal. The immune system may have acquired the selective utilization of this cytokine system, which is essential for innate antiviral immunity, to effectively couple with the induction of adaptive immunity.

Published
2003

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