研究者詳細 - 木村　宏

論文 - 木村　宏

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The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Lymphoid Neoplasms 国際共著 Open Access

Alaggio, R; Amador, C; Anagnostopoulos, I; Attygalle, AD; Araujo, IBD; Berti, E; Bhagat, G; Borges, AM; Boyer, D; Calaminici, M; Chadburn, A; Chan, JKC; Cheuk, W; Chng, WJ; Choi, JK; Chuang, SS; Coupland, SE; Czader, M; Dave, SS; de Jong, D; Du, MQ; Elenitoba-Johnson, KS; Ferry, J; Geyer, J; Gratzinger, D; Guitart, J; Gujral, S; Harris, M; Harrison, CJ; Hartmann, S; Hochhaus, A; Jansen, PM; Karube, K; Kempf, W; Khoury, J; Kimura, H; Klapper, W; Kovach, AE; Kumar, S; Lazar, AJ; Lazzi, S; Leoncini, L; Leung, N; Leventaki, V; Li, XQ; Lim, MS; Liu, WP; Louissaint, A ; Marcogliese, A; Medeiros, LJ; Michal, M; Miranda, RN; Mitteldorf, C; Montes-Moreno, S; Morice, W; Nardi, V; Naresh, KN; Natkunam, Y; Ng, SB; Oschlies, I; Ott, G; Parrens, M; Pulitzer, M; Rajkumar, SV; Rawstron, AC; Rech, K; Rosenwald, A; Said, J; Sarkozy, C; Sayed, S; Saygin, C; Schuh, A; Sewell, W; Siebert, R; Sohani, AR; Tooze, R; Traverse-Glehen, A; Vega, F; Vergier, B; Wechalekar, AD; Wood, B; Xerri, L; Xiao, WB

LEUKEMIA 36 巻 ( 7 ) 頁： 1720 - 1748 2022年7月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Leukemia

We herein present an overview of the upcoming 5th edition of the World Health Organization Classification of Haematolymphoid Tumours focussing on lymphoid neoplasms. Myeloid and histiocytic neoplasms will be presented in a separate accompanying article. Besides listing the entities of the classification, we highlight and explain changes from the revised 4th edition. These include reorganization of entities by a hierarchical system as is adopted throughout the 5th edition of the WHO classification of tumours of all organ systems, modification of nomenclature for some entities, revision of diagnostic criteria or subtypes, deletion of certain entities, and introduction of new entities, as well as inclusion of tumour-like lesions, mesenchymal lesions specific to lymph node and spleen, and germline predisposition syndromes associated with the lymphoid neoplasms.

DOI： 10.1038/s41375-022-01620-2

EBV genome variations enhance clinicopathological features of nasopharyngeal carcinoma in a non-endemic region Open Access

Kondo, S; Okuno, Y; Murata, T; Dochi, H; Wakisaka, N; Mizokami, H; Moriyama-Kita, M; Kobayashi, E; Kano, M; Komori, T; Hirai, N; Ueno, T; Nakanishi, Y; Endo, K; Sugimoto, H; Kimura, H; Yoshizaki, T

CANCER SCIENCE 113 巻 ( 7 ) 頁： 2446 - 2456 2022年7月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Cancer Science

Nasopharyngeal carcinoma (NPC) is caused by infection with Epstein–Barr virus (EBV) and endemic in certain geographic regions. EBV lytic gene, BALF2, closely associates with viral reactivation and BALF2 gene variation, the H-H-H strain, causes NPC in endemic region, southern China. Here, we investigate whether such EBV variations also affect NPC in a non-endemic region, Japan. Viral genome sequencing with 47 EBV isolates of Japanese NPC were performed and compared with those of other EBV-associated diseases from Japan or NPC in Southern China. EBV genomes of Japanese NPC are different from those of other diseases in Japan or endemic NPC; Japanese NPC was not affected by the endemic strain (the BALF2 H-H-H) but frequently carried the type 2 EBV or the strain with intermediate risk of endemic NPC (the BALF2 H-H-L). Seven single nucleotide variations were specifically associated with Japanese NPC, of which six were present in both type 1 and 2 EBV genomes, suggesting the contribution of the type 2 EBV-derived haplotype. This observation was supported by a higher viral titer and stronger viral reactivation in NPC with either type 2 or H-H-L strains. Our results highlight the importance of viral strains and viral reactivation in the pathogenesis of non-endemic NPC.

DOI： 10.1111/cas.15381

Elderly-onset systemic Epstein-Barr virus-positive T-cell lymphoma of childhood Open Access

Nishikubo, M; Hiramoto, N; Yamashita, D; Imoto, H; Sato, Y; Okuno, Y; Haga, H; Nannya, Y; Ogawa, S; Kimura, H; Ishikawa, T

PATHOLOGY INTERNATIONAL 72 巻 ( 7 ) 頁： 376 - 378 2022年7月

Epstein-Barr virus tegument protein BGLF2 in exosomes released from virus-producing cells facilitates de novo infection 国際共著 Open Access

Sato, Y; Yaguchi, M; Okuno, Y; Ishimaru, H; Sagou, K; Ozaki, S; Suzuki, T; Inagaki, T; Umeda, M; Watanabe, T; Fujimuro, M; Murata, T; Kimura, H

CELL COMMUNICATION AND SIGNALING 20 巻 ( 1 ) 頁： 95 2022年6月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Cell Communication and Signaling

Background: Viruses must adapt to the environment of their host cells to establish infection and persist. Diverse mammalian cells, including virus-infected cells, release extracellular vesicles such as exosomes containing proteins and miRNAs, and use these vesicles to mediate intercellular communication. However, the roles of exosomes in viral infection remain unclear. Results: We screened viral proteins to identify those responsible for the exosome-mediated enhancement of Epstein–Barr virus (EBV) infection. We identified BGLF2 protein encapsulated in exosomes, which were released by EBV-infected cells. BGLF2 protein is a tegument protein that exists in the space between the envelope and nucleocapsid, and it is released into the cytoplasm shortly after infection. BGLF2 protein-containing exosomes enhanced viral gene expression and repressed innate immunity, thereby supporting the EBV infection. Conclusions: The EBV tegument protein BGLF2 is encapsulated in exosomes and released by infected cells to facilitate the establishment of EBV infection. These findings suggest that tegument proteins support viral infection not only between the envelope and nucleocapsid, as well as in extraviral particles such as exosomes. Graphical abstract: [Figure not available: see fulltext.] [MediaObject not available: see fulltext.].

DOI： 10.1186/s12964-022-00902-7

EBV Exploits RNA m<SUP>6</SUP>A Modification to Promote Cell Survival and Progeny Virus Production During Lytic Cycle Open Access

Yanagi, Y; Watanabe, T; Hara, Y; Sato, Y; Kimura, H; Murata, T

FRONTIERS IN MICROBIOLOGY 13 巻頁： 870816 2022年6月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Frontiers in Microbiology

N6-methyladenosine (m6A) mediates various biological processes by affecting RNA stability, splicing, and translational efficiency. The roles of m6A modification in Epstein-Barr virus (EBV) infection in the lytic phase are unclear. Here, knockout of the m6A methyltransferase, N6-methyladenosine methyltransferase-like 3 (METTL3), or inhibition of methylation by DAA or UZH1a decreased the expression of viral lytic proteins and reduced progeny virion production. Interestingly, cell growth and viability were decreased by induction of the lytic cycle in METTL3-knockout or inhibitor-treated cells. Apoptosis was induced in those conditions possibly because of a decreased level of the anti-apoptotic viral protein, BHRF1. Therefore, m6A shows potential as a target of lytic induction therapy for EBV-associated cancers, including Burkitt lymphoma.

DOI： 10.3389/fmicb.2022.870816

PD-L1 upregulation by lytic induction of Epstein-Barr Virus Open Access

Yanagi, Y; Hara, Y; Mabuchi, S; Watanabe, T; Sato, Y; Kimura, H; Murata, T

VIROLOGY 568 巻頁： 31 - 40 2022年3月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Virology

Epstein-Barr virus (EBV) is an etiologic agent of infectious mononucleosis and several malignancies. Here, we found that reactivation of EBV resulted in increased programmed cell death-ligand 1 (PD-L1) expression in a cell type-dependent manner. Lytic induction in EBV-positive Akata, AGS, MutuI, and Jijoye cell lines increased PD-L1 levels, but cells such as EBV-negative Akata, MutuIII, and P3HR1 did not have increased PD-L1. EBV in the P3HR1 cell line has a deletion in the EBNA2 gene, while EBV in its parental cell line, Jijoye, has the complete EBNA2 gene. PD-L1 expression by lytic induction was reduced when EBNA2 was knocked down. In addition, pharmacological inhibition indicated involvement of nuclear factor kappa B, mitogen-activated protein kinase, and AKT signaling. These results suggest that EBV likely evades immunity by inducing PD-L1 upon reactivation, through the increased expression of EBNA2 and activation of signaling pathways.

DOI： 10.1016/j.virol.2022.01.006

Web of Science

Scopus

PubMed

In Silico Analysis and Synthesis of Nafamostat Derivatives and Evaluation of Their Anti-SARS-CoV-2 Activity Open Access

Fujimoto, KJ; Hobbs, DCF; Umeda, M; Nagata, A; Yamaguchi, R; Sato, Y; Sato, A; Ohmatsu, K; Ooi, T; Yanai, T; Kimura, H; Murata, T

VIRUSES-BASEL 14 巻 ( 2 ) 2022年2月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Viruses

Inhibition of transmembrane serine protease 2 (TMPRSS2) is expected to block the spike protein-mediated fusion of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Nafamostat, a potent TMPRSS2 inhibitor as well as a candidate for anti-SARS-CoV-2 drug, possesses the same acyl substructure as camostat, but is known to have a greater antiviral effect. A unique aspect of the molecular binding of nafamostat has been recently reported to be the formation of a covalent bond between its acyl substructure and Ser441 in TMPRSS2. In this study, we investigated crucial elements that cause the difference in anti-SARS-CoV-2 activity of nafamostat and camostat. In silico analysis showed that Asp435 significantly contributes to the binding of nafamostat and camostat to TMPRSS2, while Glu299 interacts strongly only with nafamostat. The estimated binding affinity for each compound with TMPRSS2 was actually consistent with the higher activity of nafamostat; however, the evaluation of the newly synthesized nafamostat derivatives revealed that the predicted binding affinity did not correlate with their anti-SARS-CoV-2 activity measured by the cytopathic effect (CPE) inhibition assay. It was further shown that the substitution of the ester bond with amide bond in nafamostat resulted in significantly weakened anti-SARS-CoV-2 activity. These results strongly indicate that the ease of covalent bond formation with Ser441 in TMPRSS2 possibly plays a major role in the anti-SARS-CoV-2 effect of nafamostat and its derivatives.

DOI： 10.3390/v14020389

Molecular Basis of Epstein-Barr Virus Latency Establishment and Lytic Reactivation 国際共著 Open Access

Murata, T; Sugimoto, A; Inagaki, T; Yanagi, Y; Watanabe, T; Sato, Y; Kimura, H

VIRUSES-BASEL 13 巻 ( 12 ) 2021年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Viruses

Epstein–Barr virus (EBV) is a causative agent of infectious mononucleosis and several types of cancer. Like other herpesviruses, it establishes an asymptomatic, life-long latent infection, with occasional reactivation and shedding of progeny viruses. During latency, EBV expresses a small number of viral genes, and exists as an episome in the host–cell nucleus. Expression patterns of latency genes are dependent on the cell type, time after infection, and milieu of the cell (e.g., germinal center or peripheral blood). Upon lytic induction, expression of the viral immediate-early genes, BZLF1 and BRLF1, are induced, followed by early gene expression, viral DNA replication, late gene expression, and maturation and egress of progeny virions. Furthermore, EBV reactivation involves more than just progeny production. The EBV life cycle is regulated by signal transduction, transcription factors, promoter sequences, epigenetics, and the 3D structure of the genome. In this article, the molecular basis of EBV latency establishment and reactivation is summarized.

DOI： 10.3390/v13122344

A STING inhibitor suppresses EBV-induced B cell transformation and lymphomagenesis 国際共著 Open Access

Miyagi, S; Watanabe, T; Hara, Y; Arata, M; Uddin, MK; Mantoku, K; Sago, K; Yanagi, Y; Suzuki, T; Al Masud, HMA; Kawada, J; Nakamura, S; Miyake, Y; Sato, Y; Murata, T; Kimura, H

CANCER SCIENCE 112 巻 ( 12 ) 頁： 5088 - 5099 2021年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Cancer Science

Epstein-Barr virus-associated lymphoproliferative disease (EBV-LPD) is frequently fatal. Innate immunity plays a key role in protecting against pathogens and cancers. The stimulator of interferon genes (STING) is regarded as a key adaptor protein allowing DNA sensors recognizing exogenous cytosolic DNA to activate the type I interferon signaling cascade. In terms of EBV tumorigenicity, the role of STING remains elusive. Here we showed that treatment with the STING inhibitor, C-176, suppressed EBV-induced transformation in peripheral blood mononuclear cells. In an EBV-LPD mouse model, C-176 treatment also inhibited tumor formation and prolonged survival. Treatment with B cells alone did not affect EBV transformation, but suppression of EBV-induced transformation was observed in the presence of T cells. Even without direct B cell-T cell contact in a transwell system, the inhibitor reduced the transformation activity, indicating that intercellular communication by humoral factors was critical to prevent EBV-induced transformation. These findings suggest that inhibition of STING signaling pathway with C-176 could be a new therapeutic target of EBV-LPD.

DOI： 10.1111/cas.15152

Web of Science

Scopus

PubMed

Deletion of Viral microRNAs in the Oncogenesis of Epstein-Barr Virus-Associated Lymphoma Open Access

Kimura, H; Okuno, Y; Sato, Y; Watanabe, T; Murata, T

FRONTIERS IN MICROBIOLOGY 12 巻頁： 667968 2021年7月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Frontiers in Microbiology

Epstein–Barr virus (EBV), which encodes >80 genes and nearly 50 non-coding RNAs, is a double-stranded DNA virus. EBV is associated with various types of lymphomas and lymphoproliferative disorders not only of B-cell but also T/NK-cell origin. However, the oncogenic mechanism remains poorly understood, including the EBV receptors expressed on T/NK cells, relationship of EBV with host genes, and epigenetic regulation of EBV and host genes. The roles of host and viral non-coding RNAs during tumorigenesis have been elucidated. EBV encodes at least 49 mature microRNAs (miRNAs), of which 44 are located in BamHI-A rightward transcripts (BARTs) region, and the remaining five are located in BamHI-H rightward fragment 1. BART miRNAs modulate cell differentiation, proliferation, apoptosis, and the cell cycle, and they are considered positive regulators of oncogenesis. We and others have recently reported that EBV-positive lymphomas frequently possess large deletions in BART miRNA clusters, suggesting that some viral miRNAs have suppressive effects on oncogenesis, and that deletion of these miRNAs may aid lymphoma formation.

DOI： 10.3389/fmicb.2021.667968

RNAseq analysis identifies involvement of EBNA2 in PD-L1 induction during Epstein-Barr virus infection of primary B cells 査読有り国際共著

Yusuke Yanagi, Yusuke Okuno, Yohei Narita, H M Abdullah Al Masud , Takahiro Watanabe , Yoshitaka Sato, Teru Kanda, Hiroshi Kimura, Takayuki Murata

Virology 557 巻頁： 44 - 54 2021年5月

Oncolytic activity of naturally attenuated herpes-simplex virus HF10 against an immunocompetent model of oral carcinoma. 査読有り

Takano G, Esaki S, Goshima F, Enomoto A, Hatano Y, Ozaki H, Watanabe T, Sato Y, Kawakita D, Murakami S, Murata T, Nishiyama Y, Iwasaki S, Kimura H.

Molecular Therapy – Oncolytics 20 巻頁： 220 - 227 2021年3月

Role of Epstein-Barr Virus C Promoter Deletion in Diffuse Large B Cell Lymphoma 査読有り国際共著

Mabuchi Seiyo, Hijioka Fumiya, Watanabe Takahiro, Yanagi Yusuke, Okuno Yusuke, Al Masud H. M. Abdullah, Sato Yoshitaka, Murata Takayuki, Kimura Hiroshi

CANCERS 13 巻 ( 3 ) 2021年2月

Direct Evidence of Abortive Lytic Infection-Mediated Establishment of Epstein-Barr Virus Latency During B-Cell Infection 査読有り国際共著

Inagaki Tomoki, Sato Yoshitaka, Ito Jumpei, Takaki Mitsuaki, Okuno Yusuke, Yaguchi Masahiro, Al Masud H. M. Abdullah, Watanabe Takahiro, Sato Kei, Iwami Shingo, Murata Takayuki, Kimura Hiroshi

FRONTIERS IN MICROBIOLOGY 11 巻 2021年1月

慢性活動性EBウイルス感染症

木村宏

日本造血細胞移植学会雑誌 10 巻 ( 2 ) 頁： 87 - 93 2021年

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：一般社団法人日本造血・免疫細胞療法学会

<p> 慢性活動性EBウイルス感染症は，EBVがT細胞あるいはNK細胞に潜伏感染し，クローナリティを持って増殖，臓器に浸潤し，多彩な症状を呈する難治性疾患である。予後は，概して不良で，無治療の場合には，臓器合併症・急性転化により死に至ることが多い。筆者らは，慢性活動性EBウイルス感染症患者に対して大規模な網羅的遺伝子解析を行い，1）生殖細胞列の変異はほとんど認められないため原発性免疫不全症が潜んでいる可能性は低いこと，2）EBV感染細胞では，DDX3X，KMT2Dなどのドライバー遺伝子変異が認められ，経時的に観察できた例では，EBV感染細胞のクローン進化が確認されること，3）高率に欠失ウイルスが認められ発症に関与している可能性があること，を明らかにした。本稿では，これら遺伝子解析によって解明されつつある慢性活動性EBウイルス感染症の発症病理と，診断・治療に関わる最新の知見について概説する。</p>

DOI： 10.7889/hct-20-026

CiNii Research

Oncolytic activity of HF10 in head and neck squamous cell carcinomas. 査読有り

Esaki S, Goshima F, Ozaki H, Takano G, Hatano Y, Kawakita D, Ijichi K, Watanabe T, Sato Y, Murata T, Iwata H, Shibamoto Y, Murakami S, Nishiyama Y, Kimura H

Cancer gene therapy 27 巻 ( 7-8 ) 頁： 585 - 598 2020年8月

Number of concomitant drugs with thrombocytopenic adverse effects and the extent inflammatory response resolution are risk factors for thrombocytopenia in patients treated with linezolid for more than 14 days 査読有り

Sato Yoshitaka, Iguchi Mitsutaka, Kato Yoshiaki, Morioka Hiroshi, Hirabayashi Aki, Tetsuka Nobuyuki, Tomita Yuka, Kato Daizo, Yamada Kiyofumi, Kimura Hiroshi, Yagi Tetsuya

NAGOYA JOURNAL OF MEDICAL SCIENCE 82 巻 ( 3 ) 頁： 407-414 2020年8月

Nationwide survey of systemic chronic active EBV infection in Japan in accordance with the new WHO classification 査読有り

Yonese Ichiro, Sakashita Chizuko, Imadome Ken-Ichi, Kobayashi Tohru, Yamamoto Masahide, Sawada Akihisa, Ito Yoshinori, Fukuhara Noriko, Hirose Asao, Takeda Yusuke, Makita Masanori, Endo Tomoyuki, Kimura Shun-Ichi, Ishimura Masataka, Miura Osamu, Ohga Shouichi, Kimura Hiroshi, Fujiwara Shigeyoshi, Arai Ayako

BLOOD ADVANCES 4 巻 ( 13 ) 頁： 2918-2926 2020年7月

A systemic form chronic active Epstein-Barr virus infection diagnosed from erythema nodosum-like skin lesions. 査読有り

Shibata A, Ishiguro Y, Makita S, Yamaga Y, Kimura H, Akiyama M

European journal of dermatology : EJD 30 巻 ( 3 ) 頁： 314-316 2020年6月

Epstein-Barr virus NK and T cell lymphoproliferative disease: report of a 2018 international meeting 査読有り国際共著

Cohena Jeffrey I., Iwatsuki Keiji, Ko Young-Hyeh, Kimura Hiroshi, Manoli Irini, Ohshima Koichi, Pittaluga Stefania, Quintanilla-Martinez Leticia, Jaffe Elaine S.

LEUKEMIA & LYMPHOMA 61 巻 ( 4 ) 頁： 808-819 2020年3月

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