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5. Characterization of SARS-CoV-2 Omicron BA.2.75 clinical isolates

Author

Uraki, Ryuta, Iida, Shun, Halfmann, Peter J., Yamayoshi, Seiya, Hirata, Yuichiro, Iwatsuki-Horimoto, Kiyoko, Kiso, Maki, Ito, Mutsumi, Furusawa, Yuri, Ueki, Hiroshi, Sakai-Tagawa, Yuko, Kuroda, Makoto, Maemura, Tadashi, Kim, Taksoo, Mine, Sohtaro, Iwamoto, Noriko, Li, Rong, Liu, Yanan, Larson, Deanna, Fukushi, Shuetsu, Watanabe, Shinji, Maeda, Ken, Wang, Zhongde, Ohmagari, Norio, Theiler, James, Fischer, Will, Korber, Bette, Imai, Masaki, Suzuki, Tadaki, and Kawaoka, Yoshihiro

Published
2023
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6. Identification of SARS-CoV-2 Mpro inhibitors containing P1’ 4-fluorobenzothiazole moiety highly active against SARS-CoV-2

Author

Higashi-Kuwata, Nobuyo, Tsuji, Kohei, Hayashi, Hironori, Bulut, Haydar, Kiso, Maki, Imai, Masaki, Ogata-Aoki, Hiromi, Ishii, Takahiro, Kobayakawa, Takuya, Nakano, Kenta, Takamune, Nobutoki, Kishimoto, Naoki, Hattori, Shin-ichiro, Das, Debananda, Uemura, Yukari, Shimizu, Yosuke, Aoki, Manabu, Hasegawa, Kazuya, Suzuki, Satoshi, Nishiyama, Akie, Saruwatari, Junji, Shimizu, Yukiko, Sukenaga, Yoshikazu, Takamatsu, Yuki, Tsuchiya, Kiyoto, Maeda, Kenji, Yoshimura, Kazuhisa, Iida, Shun, Ozono, Seiya, Suzuki, Tadaki, Okamura, Tadashi, Misumi, Shogo, Kawaoka, Yoshihiro, Tamamura, Hirokazu, and Mitsuya, Hiroaki

Published
2023
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9. Characterization of SARS-CoV-2 Omicron BA.4 and BA.5 isolates in rodents

Author

Uraki, Ryuta, Halfmann, Peter J., Iida, Shun, Yamayoshi, Seiya, Furusawa, Yuri, Kiso, Maki, Ito, Mutsumi, Iwatsuki-Horimoto, Kiyoko, Mine, Sohtaro, Kuroda, Makoto, Maemura, Tadashi, Sakai-Tagawa, Yuko, Ueki, Hiroshi, Li, Rong, Liu, Yanan, Larson, Deanna, Fukushi, Shuetsu, Watanabe, Shinji, Maeda, Ken, Pekosz, Andrew, Kandeil, Ahmed, Webby, Richard J., Wang, Zhongde, Imai, Masaki, Suzuki, Tadaki, and Kawaoka, Yoshihiro

Published
2022
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12. Characterization and antiviral susceptibility of SARS-CoV-2 Omicron BA.2

Author

Uraki, Ryuta, Kiso, Maki, Iida, Shun, Imai, Masaki, Takashita, Emi, Kuroda, Makoto, Halfmann, Peter J., Loeber, Samantha, Maemura, Tadashi, Yamayoshi, Seiya, Fujisaki, Seiichiro, Wang, Zhongde, Ito, Mutsumi, Ujie, Michiko, Iwatsuki-Horimoto, Kiyoko, Furusawa, Yuri, Wright, Ryan, Chong, Zhenlu, Ozono, Seiya, Yasuhara, Atsuhiro, Ueki, Hiroshi, Sakai-Tagawa, Yuko, Li, Rong, Liu, Yanan, Larson, Deanna, Koga, Michiko, Tsutsumi, Takeya, Adachi, Eisuke, Saito, Makoto, Yamamoto, Shinya, Hagihara, Masao, Mitamura, Keiko, Sato, Tetsuro, Hojo, Masayuki, Hattori, Shin-ichiro, Maeda, Kenji, Valdez, Riccardo, Okuda, Moe, Murakami, Jurika, Duong, Calvin, Godbole, Sucheta, Douek, Daniel C., Maeda, Ken, Watanabe, Shinji, Gordon, Aubree, Ohmagari, Norio, Yotsuyanagi, Hiroshi, Diamond, Michael S., Hasegawa, Hideki, Mitsuya, Hiroaki, Suzuki, Tadaki, and Kawaoka, Yoshihiro

Published
2022
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13. Characterization of a new SARS-CoV-2 variant that emerged in Brazil

Author

Imai, Masaki, Halfmann, Peter J., Yamayoshi, Seiya, Iwatsuki-Horimoto, Kiyoko, Chiba, Shiho, Watanabe, Tokiko, Nakajima, Noriko, Ito, Mutsumi, Kuroda, Makoto, Kiso, Maki, Maemura, Tadashi, Takahashi, Kenta, Loeber, Samantha, Hatta, Masato, Koga, Michiko, Nagai, Hiroyuki, Yamamoto, Shinya, Saito, Makoto, Adachi, Eisuke, Akasaka, Osamu, Nakamura, Morio, Nakachi, Ichiro, Ogura, Takayuki, Baba, Rie, Fujita, Kensuke, Ochi, Junichi, Mitamura, Keiko, Kato, Hideaki, Nakajima, Hideaki, Yagi, Kazuma, Hattori, Shin-ichiro, Maeda, Kenji, Suzuki, Tetsuya, Miyazato, Yusuke, Valdez, Riccardo, Gherasim, Carmen, Furusawa, Yuri, Okuda, Moe, Ujie, Michiko, Lopes, Tiago J. S., Yasuhara, Atsuhiro, Ueki, Hiroshi, Sakai-Tagawa, Yuko, Eisfeld, Amie J., Baczenas, John J., Baker, David A., O’Connor, Shelby L., O’Connor, David H., Fukushi, Shuetsu, Fujimoto, Tsuguto, Kuroda, Yudai, Gordon, Aubree, Maeda, Ken, Ohmagari, Norio, Sugaya, Norio, Yotsuyanagi, Hiroshi, Mitsuya, Hiroaki, Suzuki, Tadaki, and Kawaoka, Yoshihiro

Published
2021

14. SARS-CoV-2 Omicron virus causes attenuated disease in mice and hamsters

Author

Halfmann, Peter J., Iida, Shun, Iwatsuki-Horimoto, Kiyoko, Maemura, Tadashi, Kiso, Maki, Scheaffer, Suzanne M., Darling, Tamarand L., Joshi, Astha, Loeber, Samantha, Singh, Gagandeep, Foster, Stephanie L., Ying, Baoling, Case, James Brett, Chong, Zhenlu, Whitener, Bradley, Moliva, Juan, Floyd, Katharine, Ujie, Michiko, Nakajima, Noriko, Ito, Mutsumi, Wright, Ryan, Uraki, Ryuta, Warang, Prajakta, Gagne, Matthew, Li, Rong, Sakai-Tagawa, Yuko, Liu, Yanan, Larson, Deanna, Osorio, Jorge E., Hernandez-Ortiz, Juan P., Henry, Amy R., Ciuoderis, Karl, Florek, Kelsey R., Patel, Mit, Odle, Abby, Wong, Lok-Yin Roy, Bateman, Allen C., Wang, Zhongde, Edara, Venkata-Viswanadh, Chong, Zhenlu, Franks, John, Jeevan, Trushar, Fabrizio, Thomas, DeBeauchamp, Jennifer, Kercher, Lisa, Seiler, Patrick, Gonzalez-Reiche, Ana Silvia, Sordillo, Emilia Mia, Chang, Lauren A., van Bakel, Harm, Simon, Viviana, Douek, Daniel C., Sullivan, Nancy J., Thackray, Larissa B., Ueki, Hiroshi, Yamayoshi, Seiya, Imai, Masaki, Perlman, Stanley, Webby, Richard J., Seder, Robert A., Suthar, Mehul S., García-Sastre, Adolfo, Schotsaert, Michael, Suzuki, Tadaki, Boon, Adrianus C. M., Diamond, Michael S., and Kawaoka, Yoshihiro

Published
2022
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16. Syrian hamsters as a small animal model for SARS-CoV-2 infection and countermeasure development

Author

Imai, Masaki, Iwatsuki-Horimoto, Kiyoko, Hatta, Masato, Loeber, Samantha, Halfmann, Peter J., Nakajima, Noriko, Watanabe, Tokiko, Ujie, Michiko, Takahashi, Kenta, Ito, Mutsumi, Yamada, Shinya, Fan, Shufang, Chiba, Shiho, Kuroda, Makoto, Guan, Lizheng, Takada, Kosuke, Armbrust, Tammy, Balogh, Aaron, Furusawa, Yuri, Okuda, Moe, Ueki, Hiroshi, Yasuhara, Atsuhiro, Sakai-Tagawa, Yuko, Lopes, Tiago J. S., Kiso, Maki, Yamayoshi, Seiya, Kinoshita, Noriko, Ohmagari, Norio, Hattori, Shin-ichiro, Takeda, Makoto, Mitsuya, Hiroaki, Krammer, Florian, Suzuki, Tadaki, and Kawaoka, Yoshihiro

Published
2020

17. ACE2-like carboxypeptidase B38-CAP protects from SARS-CoV-2-induced lung injury

Author

Yamaguchi, Tomokazu, Hoshizaki, Midori, Minato, Takafumi, Nirasawa, Satoru, Asaka, Masamitsu N., Niiyama, Mayumi, Imai, Masaki, Uda, Akihiko, Chan, Jasper Fuk-Woo, Takahashi, Saori, An, Jianbo, Saku, Akari, Nukiwa, Ryota, Utsumi, Daichi, Kiso, Maki, Yasuhara, Atsuhiro, Poon, Vincent Kwok-Man, Chan, Chris Chung-Sing, Fujino, Yuji, Motoyama, Satoru, Nagata, Satoshi, Penninger, Josef M., Kamada, Haruhiko, Yuen, Kwok-Yung, Kamitani, Wataru, Maeda, Ken, Kawaoka, Yoshihiro, Yasutomi, Yasuhiro, Imai, Yumiko, and Kuba, Keiji

Published
2021
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18. Influenza A variants with reduced susceptibility to baloxavir isolated from Japanese patients are fit and transmit through respiratory droplets

Author

Imai, Masaki, Yamashita, Makoto, Sakai-Tagawa, Yuko, Iwatsuki-Horimoto, Kiyoko, Kiso, Maki, Murakami, Jurika, Yasuhara, Atsuhiro, Takada, Kosuke, Ito, Mutsumi, Nakajima, Noriko, Takahashi, Kenta, Lopes, Tiago J. S., Dutta, Jayeeta, Khan, Zenab, Kriti, Divya, van Bakel, Harm, Tokita, Akifumi, Hagiwara, Haruhisa, Izumida, Naomi, Kuroki, Haruo, Nishino, Tamon, Wada, Noriyuki, Koga, Michiko, Adachi, Eisuke, Jubishi, Daisuke, Hasegawa, Hideki, and Kawaoka, Yoshihiro

Published
2020
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19. Development of a Mouse-Adapted Reporter SARS-CoV-2 as a Tool for Two-Photon In Vivo Imaging.

Author

Ueki, Hiroshi, Kiso, Maki, Furusawa, Yuri, Iida, Shun, Yamayoshi, Seiya, Nakajima, Noriko, Imai, Masaki, Suzuki, Tadaki, and Kawaoka, Yoshihiro

Subjects
*SARS-CoV-2, *COVID-19
Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) often causes severe viral pneumonia. Although many studies using mouse models have examined the pathogenicity of SARS-CoV-2, COVID-19 pathogenesis remains poorly understood. In vivo imaging analysis using two-photon excitation microscopy (TPEM) is useful for elucidating the pathology of COVID-19, providing pathological insights that are not available from conventional histological analysis. However, there is no reporter SARS-CoV-2 that demonstrates pathogenicity in C57BL/6 mice and emits sufficient light intensity for two-photon in vivo imaging. Here, we generated a mouse-adapted strain of SARS-CoV-2 (named MASCV2-p25) and demonstrated its efficient replication in the lungs of C57BL/6 mice, causing fatal pneumonia. Histopathologic analysis revealed the severe inflammation and infiltration of immune cells in the lungs of MASCV2-p25-infected C57BL/6 mice, not unlike that observed in COVID-19 patients with severe pneumonia. Subsequently, we generated a mouse-adapted reporter SARS-CoV-2 (named MASCV-Venus-p9) by inserting the fluorescent protein-encoding gene Venus into MASCV2-p25 and sequential lung-to-lung passages in C57BL/6 mice. C57BL/6 mice infected with MASCV2-Venus-p9 exhibited severe pneumonia. In addition, the TPEM of the lungs of the infected C57BL/6J mice showed that the infected cells emitted sufficient levels of fluorescence for easy observation. These findings suggest that MASCV2-Venus-p9 will be useful for two-photon in vivo imaging studies of the pathogenesis of severe COVID-19 pneumonia. [ABSTRACT FROM AUTHOR]

Published
2024
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23. Emergence of Oseltamivir-Resistant H7N9 Influenza Viruses in Immunosuppressed Cynomolgus Macaques

Author

Kiso, Maki, Iwatsuki-Horimoto, Kiyoko, Yamayoshi, Seiya, Uraki, Ryuta, Ito, Mutsumi, Nakajima, Noriko, Yamada, Shinya, Imai, Masaki, Kawakami, Eiryo, Tomita, Yuriko, Fukuyama, Satoshi, Itoh, Yasushi, Ogasawara, Kazumasa, Lopes, Tiago J. S., Watanabe, Tokiko, Moncla, Louise H., Hasegawa, Hideki, Friedrich, Thomas C., Neumann, Gabriele, and Kawaoka, Yoshihiro

Published
2017

25. Characterization of a Feline Influenza A(H7N2) Virus

Author

Hatta, Masato, Zhong, Gongxun, Gao, Yuwei, Nakajima, Noriko, Fan, Shufang, Chiba, Shiho, Deering, Kathleen M., Ito, Mutsumi, Imai, Masaki, Kiso, Maki, Nakatsu, Sumiho, Lopes, Tiago J., Thompson, Andrew J., McBride, Ryan, Suarez, David L., Macken, Catherine A., Sugita, Shigeo, Neumann, Gabriele, Hasegawa, Hideki, Paulson, James C., Toohey-Kurth, Kathy L., and Kawaoka, Yoshihiro

Subjects
Influenza viruses -- Research, Disease transmission -- Research, Virus replication -- Research, Cat diseases -- Research, Health
Abstract

Influenza A viruses are endemic in humans and enzootic in other mammalian species including swine and horses; occasional infections of other mammalian species including whales, seals, sea lions, felidae in [...]

Published
2018
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28. Efficacy of favipiravir against influenza virus resistant to both baloxavir and neuraminidase inhibitors.

Author

Kiso, Maki, Yamayoshi, Seiya, and Kawaoka, Yoshihiro

Subjects
*NEURAMINIDASE, *INFLUENZA viruses, *REVERSE genetics, *VIRUS diseases, *PUBLIC health, *VIRAL replication
Abstract

Objectives Widespread resistance of influenza viruses to neuraminidase (NA) inhibitor or polymerase inhibitor, baloxavir, is a major public health concern. The amino acid mutations R152K in NA and I38T in polymerase acidic (PA) are responsible for resistance to NA inhibitors and baloxavir, respectively. Methods We generated recombinant A(H1N1)pdm09 viruses possessing NA-R152K, PA-I38T or both mutations by using a plasmid-based reverse genetics system, characterized their virological properties in vitro and in vivo , and examined whether oseltamivir, baloxavir and favipiravir are effective against these mutant viruses. Results The three mutant viruses showed similar or superior growth kinetics and virulence to those of wild-type virus. Although oseltamivir and baloxavir blocked the replication of the wild-type virus in vitro , oseltamivir and baloxavir failed to suppress the replication of the NA-R152K and PA-I38T viruses in vitro , respectively. Mutant virus possessing both mutations grew in the presence of oseltamivir or baloxavir in vitro. Baloxavir treatment protected mice from lethal infection with wild-type or NA-R152K virus, but failed to protect mice from lethal infection with PA-I38T or PA-I38T/NA-R152K virus. Favipiravir treatment protected mice from lethal infection with all viruses tested, whereas oseltamivir treatment did not protect at all. Conclusions Our findings indicate that favipiravir should be used to treat patients with suspected baloxavir-resistant virus infection. [ABSTRACT FROM AUTHOR]

Published
2023
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29. In vitro and in vivo characterization of SARS-CoV-2 strains resistant to nirmatrelvir.

Author

Kiso, Maki, Furusawa, Yuri, Uraki, Ryuta, Imai, Masaki, Yamayoshi, Seiya, and Kawaoka, Yoshihiro

Subjects
SARS-CoV-2 Omicron variant, SARS-CoV-2 Delta variant, SARS-CoV-2, ANTIVIRAL agents, PUBLIC health
Abstract

Nirmatrelvir, an oral antiviral agent that targets a SARS-CoV-2 main protease (3CLpro), is clinically useful against infection with SARS-CoV-2 including its omicron variants. Since most omicron subvariants have reduced sensitivity to many monoclonal antibody therapies, potential SARS-CoV-2 resistance to nirmatrelvir is a major public health concern. Several amino acid substitutions have been identified as being responsible for reduced susceptibility to nirmatrelvir. Among them, we selected L50F/E166V and L50F/E166A/L167F in the 3CLpro because these combinations of substitutions are unlikely to affect virus fitness. We prepared and characterized delta variants possessing Nsp5-L50F/E166V and Nsp5-L50F/E166A/L167F. Both mutant viruses showed decreased susceptibility to nirmatrelvir and their growth in VeroE6/TMPRSS2 cells was delayed. Both mutant viruses showed attenuated phenotypes in a male hamster infection model, maintained airborne transmissibility, and were outcompeted by wild-type virus in co-infection experiments in the absence of nirmatrelvir, but less so in the presence of the drug. These results suggest that viruses possessing Nsp5-L50F/E166V and Nsp5-L50F/E166A/L167F do not become dominant in nature. However, it is important to closely monitor the emergence of nirmatrelvir-resistant SARS-CoV-2 variants because resistant viruses with additional compensatory mutations could emerge, outcompete the wild-type virus, and become dominant. Resistance to nirmatrelvir, an oral antiviral agent that targets SARS-CoV-2 and is clinically useful against infection with Omicron variants, is currently not well understood. In this study, the authors characterize mutant viruses with reduced sensitivity to nirmatrelvir in vitro and in vivo. [ABSTRACT FROM AUTHOR]

Published
2023
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31. Identification of SARS-CoV-2 Mpro inhibitors containing P1' 4-fluorobenzothiazole moiety highly active against SARS-CoV-2.

Author

Higashi-Kuwata, Nobuyo, Tsuji, Kohei, Hayashi, Hironori, Bulut, Haydar, Kiso, Maki, Imai, Masaki, Ogata-Aoki, Hiromi, Ishii, Takahiro, Kobayakawa, Takuya, Nakano, Kenta, Takamune, Nobutoki, Kishimoto, Naoki, Hattori, Shin-ichiro, Das, Debananda, Uemura, Yukari, Shimizu, Yosuke, Aoki, Manabu, Hasegawa, Kazuya, Suzuki, Satoshi, and Nishiyama, Akie

Subjects
SARS-CoV-2 Omicron variant, SARS-CoV-2 Delta variant, SARS-CoV-2, MOIETIES (Chemistry), SMALL molecules
Abstract

COVID-19 caused by SARS-CoV-2 has continually been serious threat to public health worldwide. While a few anti-SARS-CoV-2 therapeutics are currently available, their antiviral potency is not sufficient. Here, we identify two orally available 4-fluoro-benzothiazole-containing small molecules, TKB245 and TKB248, which specifically inhibit the enzymatic activity of main protease (Mpro) of SARS-CoV-2 and significantly more potently block the infectivity and replication of various SARS-CoV-2 strains than nirmatrelvir, molnupiravir, and ensitrelvir in cell-based assays employing various target cells. Both compounds also block the replication of Delta and Omicron variants in human-ACE2-knocked-in mice. Native mass spectrometric analysis reveals that both compounds bind to dimer Mpro, apparently promoting Mpro dimerization. X-ray crystallographic analysis shows that both compounds bind to Mpro's active-site cavity, forming a covalent bond with the catalytic amino acid Cys-145 with the 4-fluorine of the benzothiazole moiety pointed to solvent. The data suggest that TKB245 and TKB248 might serve as potential therapeutics for COVID-19 and shed light upon further optimization to develop more potent and safer anti-SARS-CoV-2 therapeutics. Effective antivirals are critical for combatting SARS-CoV-2 infections. Here, the authors develop two orally available small molecules, which specifically inhibit the activity of the SARS-CoV-2 main protease and potently block the infectivity and replication of various SARS-CoV-2 strains in cells and mice. [ABSTRACT FROM AUTHOR]

Published
2023
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35. Characterization of H7N9 influenza A viruses isolated from humans

Author

Watanabe, Tokiko, Kiso, Maki, Fukuyama, Satoshi, Nakajima, Noriko, Imai, Masaki, Yamada, Shinya, Murakami, Shin, Yamayoshi, Seiya, Iwatsuki-Horimoto, Kiyoko, Sakoda, Yoshihiro, Takashita, Emi, McBride, Ryan, Noda, Takeshi, Hatta, Masato, Imai, Hirotaka, Zhao, Dongming, Kishida, Noriko, Shirakura, Masayuki, de Vries, Robert P., Shichinohe, Shintaro, Okamatsu, Masatoshi, Tamura, Tomokazu, Tomita, Yuriko, Fujimoto, Naomi, Goto, Kazue, Katsura, Hiroaki, Kawakami, Eiryo, Ishikawa, Izumi, Watanabe, Shinji, Ito, Mutsumi, Sakai-Tagawa, Yuko, Sugita, Yukihiko, Uraki, Ryuta, Yamaji, Reina, Eisfeld, Amie J., Zhong, Gongxun, Fan, Shufang, Ping, Jihui, Maher, Eileen A., Hanson, Anthony, Uchida, Yuko, Saito, Takehiko, Ozawa, Makoto, Neumann, Gabriele, Kida, Hiroshi, Odagiri, Takato, Paulson, James C., Hasegawa, Hideki, Tashiro, Masato, and Kawaoka, Yoshihiro

Published
2013
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36. Highly pathogenic avian influenza virus infection in feral raccoons, Japan

Author

Horimoto, Taisuke, Maeda, Ken, Murakami, Shin, Kiso, Maki, Iwatsuki-Horimoto, Kiyoko, Sashika, Mariko, Ito, Toshihiro, Suzuki, Kazuo, Yokoyama, Mayumi, and Kawaoka, Yoshihiro

Subjects
Avian influenza -- Research -- Causes of, Avian influenza viruses -- Health aspects -- Research, Disease transmission -- Research, Raccoons -- Health aspects -- Research, Health
Abstract

Although all known subtypes of influenza A virus are maintained in waterfowl, these viruses have also been isolated from various avian and mammalian species. In particular, numerous reports have been [...]

Published
2011
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38. In vitro and in vivo characterization of new swine-origin H1N1 influenza viruses

Author

Itoh, Yasushi, Shinya, Kyoko, Kiso, Maki, Watanabe, Tokiko, Sakoda, Yoshihiro, Hatta, Masato, Muramoto, Yukiko, Tamura, Daisuke, Sakai-Tagawa, Yuko, Noda, Takeshi, Sakabe, Saori, Imai, Masaki, Hatta, Yasuko, Watanabe, Shinji, Li, Chengjun, Yamada, Shinya, Fujii, Ken, Murakami, Shin, Imai, Hirotaka, Kakugawa, Satoshi, Ito, Mutsumi, Takano, Ryo, Iwatsuki-Horimoto, Kiyoko, Shimojima, Masayuki, Horimoto, Taisuke, Goto, Hideo, Takahashi, Kei, Makino, Akiko, Ishigaki, Hirohito, Nakayama, Misako, Okamatsu, Masatoshi, Takahashi, Kazuo, Warshauer, David, Shult, Peter A., Saito, Reiko, Suzuki, Hiroshi, Furuta, Yousuke, Yamashita, Makoto, Mitamura, Keiko, Nakano, Kunio, Nakamura, Morio, Brockman-Schneider, Rebecca, Mitamura, Hiroshi, Yamazaki, Masahiko, Sugaya, Norio, Suresh, M., Ozawa, Makoto, Neumann, Gabriele, Gern, James, Kida, Hiroshi, Ogasawara, Kazumasa, and Kawaoka, Yoshihiro

Published
2009
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39. Emergence of influenza B viruses with reduced sensitivity to neuraminidase inhibitors

Author

Hatakeyama, Shuji, Sugaya, Norio, Ito, Mutsumi, Yamazaki, Masahiko, Ichikawa, Masatak, Kimura, Kazuhiro, Kiso, Maki, Shimizu, Hideaki, Kawakami, Chiharu, Koike, Kazuhiko, Mitamura, Keiko, and Kawaoka, Yoshihiro

Subjects
Influenza viruses -- Research, Viral drug resistance -- Research, Zanamivir -- Research, Zanamivir -- Health aspects
Abstract

The prevalence and transmissibility of influenza B viruses with reduced sensitivity to neuraminidase inhibitors was assessed at four community hospitals in Japan during the 2004-2005 influenza seasons. The results demonstrated that influenza B viruses with reduced sensitivity to neuraminidase inhibitors could emerge during routine therapy, appearing to be transmitted from person to person.

Published
2007

41. Haemagglutinin mutations responsible for the binding of H5N1 influenza A viruses to human-type receptors

Author

Yamada, Shinya, Suzuki, Yasuo, Suzuki, Takashi, Le, Mai Q., Nidom, Chairul A., Sakai-Tagawa, Yuko, Muramoto, Yukiko, Ito, Mutsumi, Kiso, Maki, Horimoto, Taisuke, Shinya, Kyoko, Sawada, Toshihiko, Kiso, Makoto, Usui, Taiichi, Murata, Takeomi, Lin, Yipu, Hay, Alan, Haire, Lesley F., Stevens, David J., Russell, Rupert J., Gamblin, Steven J., Skehel, John J., and Kawaoka, Yoshihiro

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

Author(s): Shinya Yamada [1, 3]; Yasuo Suzuki [3, 4]; Takashi Suzuki [3, 5]; Mai Q. Le [6]; Chairul A. Nidom [7]; Yuko Sakai-Tagawa [1, 3]; Yukiko Muramoto [1, 3]; Mutsumi [...]

Published
2006
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43. AVIAN FLU: Isolation of drug-resistant H5N1 virus

Author

Le, Q. Mai, Kiso, Maki, Someya, Kazuhiko, Sakai, Yuko T., Nguyen, T. Hien, Nguyen, Khan H. L., Pham, N. Dinh, Ngyen, Ha H., Yamada, Shinya, Muramoto, Yukiko, Horimoto, Taisuke, Takada, Ayato, Goto, Hideo, Suzuki, Takashi, Suzuki, Yasuo, and Kawaoka, Yoshihiro

Published
2005

44. Pathogenesis of Influenza A(H7N9) Virus in Aged Nonhuman Primates.

Author

Fukuyama, Satoshi, Iwatsuki-Horimoto, Kiyoko, Kiso, Maki, Nakajima, Noriko, Gregg, Robert W, Katsura, Hiroaki, Tomita, Yuriko, Maemura, Tadashi, Lopes, Tiago Jose da Silva, Watanabe, Tokiko, Shoemaker, Jason E, Hasegawa, Hideki, Yamayoshi, Seiya, Kawaoka, Yoshihiro, and da Silva Lopes, Tiago Jose

Subjects
PATHOLOGY, OLDER patients, AVIAN influenza, INFLUENZA, VIRUS diseases, H7N9 Influenza, ORTHOMYXOVIRUS infections, BIOLOGICAL models, CYTOKINES, RESEARCH, INFLUENZA A virus, LUNGS, ANIMAL experimentation, RESEARCH methodology, MEDICAL cooperation, EVALUATION research, PRIMATES, COMPARATIVE studies, AGING
Abstract

The avian influenza A(H7N9) virus has caused high mortality rates in humans, especially in the elderly; however, little is known about the mechanistic basis for this. In the current study, we used nonhuman primates to evaluate the effect of aging on the pathogenicity of A(H7N9) virus. We observed that A(H7N9) virus infection of aged animals (defined as age 20-26 years) caused more severe symptoms than infection of young animals (defined as age 2-3 years). In aged animals, lung inflammation was weak and virus infection was sustained. Although cytokine and chemokine expression in the lungs of most aged animals was lower than that in the lungs of young animals, 1 aged animal showed severe symptoms and dysregulated proinflammatory cytokine and chemokine production. These results suggest that attenuated or dysregulated immune responses in aged animals are responsible for the severe symptoms observed among elderly patients infected with A(H7N9) virus. [ABSTRACT FROM AUTHOR]

Published
2020
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45. Baloxavir Marboxil Treatment of Nude Mice Infected With Influenza A Virus.

Author

Kiso, Maki, Yamayoshi, Seiya, Murakami, Jurika, and Kawaoka, Yoshihiro

Subjects
*INFLUENZA A virus, *RESPIRATORY organs, *WEIGHT loss, *MICE, *NUDITY, *ANIMAL experimentation, *ANTIVIRAL agents, *COMPARATIVE studies, *DOSE-effect relationship in pharmacology, *HETEROCYCLIC compounds, *RESEARCH methodology, *MEDICAL cooperation, *PYRIDINE, *RESEARCH, *EVALUATION research, *ORTHOMYXOVIRUS infections
Abstract

Background: Immunocompromised patients infected with influenza virus require prolonged treatment with neuraminidase inhibitors, because these patients are not able to eradicate the virus from the respiratory tract, leading to the emergence of drug-resistant mutant viruses.Methods: In this study, we examined the efficacy of baloxavir marboxil in nude mice that were immunologically deficient.Results: Daily treatment with a suboptimal dose of baloxavir marboxil increased the survival time of the virus-infected nude mice but did not clear the virus from their respiratory organs, resulting in gradual body weight loss after termination of treatment.Conclusions: Despite the prolonged baloxavir marboxil treatment, few resistant mutants were detected. [ABSTRACT FROM AUTHOR]

Published
2020
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46. Characterization of H7N9 avian influenza viruses isolated from duck meat products.

Author

Wu, Li, Mitake, Hiromichi, Kiso, Maki, Ito, Mutsumi, Iwatsuki‐Hirimoto, Kiyoko, Yamayoshi, Seiya, Lopes, Tiago J. S., Feng, Huapeng, Sumiyoshi, Riho, Shibata, Akihiro, Osaka, Hiroyuki, Imai, Masaki, Watanabe, Tokiko, and Kawaoka, Yoshihiro

Subjects
INFLUENZA A virus, H7N9 subtype, AVIAN influenza, AVIAN influenza A virus, MEAT, DUCKS as food
Abstract

Avian influenza H7N9 viruses have caused five epidemic waves of human infections since the first human cases were reported in 2013. In 2016, the initial low pathogenic avian influenza (LPAI) H7N9 viruses became highly pathogenic, acquiring multi‐basic amino acids at the haemagglutinin cleavage site. These highly pathogenic avian influenza (HPAI) H7N9 viruses have been detected in poultry and humans in China, causing concerns of a serious threat to global public health. In Japan, both HPAI and LPAI H7N9 viruses were isolated from duck meat products carried illegally and relinquished voluntarily at the border by passengers on flights from China to Japan between 2016 and 2017. Some of the LPAI and HPAI H7N9 viruses detected at the border in Japan were characterized previously in chickens and ducks; however, their pathogenicity and replicative ability in mammals remain unknown. In this study, we assessed the biological features of two HPAI H7N9 virus isolates [A/duck/Japan/AQ‐HE29‐22/2017 (HE29‐22) and A/duck/Japan/AQ‐HE29‐52/2017 (HE29‐52); both of these viruses were isolated from duck meat at the border)] and an LPAI H7N9 virus isolate [A/duck/Japan/AQ‐HE28‐3/2016 (HE28‐3)] in mice and ferrets. In mice, HE29‐52 was more pathogenic than HE29‐22 and HE28‐3. In ferrets, the two HPAI virus isolates replicated more efficiently in the lower respiratory tract of the animals than did the LPAI virus isolate. Our results indicate that HPAI H7N9 viruses with the potential to cause severe diseases in mammals have been illegally introduced to Japan. [ABSTRACT FROM AUTHOR]

Published
2020
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47. Characterization of a SARS-CoV-2 EG.5.1 clinical isolate in vitro and in vivo.

Author

Uraki, Ryuta, Kiso, Maki, Iwatsuki-Horimoto, Kiyoko, Yamayoshi, Seiya, Ito, Mutsumi, Chiba, Shiho, Sakai-Tagawa, Yuko, Imai, Masaki, Kashima, Yukie, Koga, Michiko, Fuwa, Noriko, Okumura, Nobumasa, Hojo, Masayuki, Iwamoto, Noriko, Kato, Hideaki, Nakajima, Hideaki, Ohmagari, Norio, Yotsuyanagi, Hiroshi, Suzuki, Yutaka, and Kawaoka, Yoshihiro

Abstract

EG.5.1 is a subvariant of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron XBB variant that is rapidly increasing in prevalence worldwide. However, the pathogenicity, transmissibility, and immune evasion properties of isolates of EG.5.1 are largely unknown. Here, we show that there are no obvious differences in growth ability and pathogenicity between EG.5.1 and XBB.1.5 in hamsters. We also demonstrate that, like XBB.1.5, EG.5.1 is transmitted more efficiently between hamsters compared to its predecessor, BA.2. In contrast, unlike XBB.1.5, we detect EG.5.1 in the lungs of four of six exposed hamsters, suggesting that the virus properties of EG.5.1 are different from those of XBB.1.5. Finally, we find that the neutralizing activity of plasma from convalescent individuals against EG.5.1 was slightly, but significantly, lower than that against XBB.1.5 or XBB.1.9.2. Our data suggest that the different virus properties after transmission and the altered antigenicity of EG.5.1 may be driving its increasing prevalence over XBB.1.5 in humans. [Display omitted] • EG.5.1 and XBB.1.5 show similar growth ability and pathogenicity in hamsters • Unlike XBB.1.5, infectious EG.5.1 is detected in the lungs of some EG.5.1-exposed hamsters • Immune-evading properties of EG.5.1 are significantly enhanced relative to those of XBB.1.5 Uraki et al. find infectious EG.5.1, but not XBB.1.5, in the lungs of some variant-exposed hamsters in airborne transmission studies, despite similar growth and pathogenicity between EG.5.1 and XBB.1.5. EG.5.1 also exhibits superior immune-evading properties compared to XBB.1.5. [ABSTRACT FROM AUTHOR]

Published
2023
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48. Resistant influenza A viruses in children treated with oseltamivir: descriptive study

Author

Kiso, Maki, Mitamura, Keiko, Sakai-Tagawa, Yuko, Shiraishi, Kyoko, Kawakami, Chiharu, Kimura, Kazuhiro, Hayden, Frederick G., Sugaya, Norio, and Kawaoka, Yoshihiro

Subjects
Oseltamivir (Medication) -- Dosage and administration, Oseltamivir (Medication) -- Research, Influenza viruses -- Research, Influenza viruses -- Drug therapy
Published
2004

49. The Marmoset as an Animal Model of Influenza: Infection With A(H1N1)pdm09 and Highly Pathogenic A(H5N1) Viruses via the Conventional or Tracheal Spray Route.

Author

Iwatsuki-Horimoto, Kiyoko, Nakajima, Noriko, Kiso, Maki, Takahashi, Kenta, Ito, Mutsumi, Inoue, Takashi, Horiuchi, Machiko, Okahara, Norio, Sasaki, Erika, Hasegawa, Hideki, and Kawaoka, Yoshihiro

Subjects
H1N1 influenza, H5N1 Influenza, INFLAMMATION
Abstract

To control infectious diseases in humans, it is important to understand the pathogenicity of the infecting organism(s). Although non-human primates, such as cynomolgus and rhesus macaques, have been used for influenza virus infection models, their size can limit their use in confined animal facilities. In this study, we investigated the susceptibility of marmosets to influenza viruses to assess the possibility of using these animals as a non-human primate model for influenza research. We first used an influenza A (H1N1)pdm09 virus to compare two inoculation routes: the conventional route, via a combination of the intratracheal, intranasal, ocular, and oral routes; and the tracheal spray route. In marmosets inoculated via the tracheal spray route, we found inflammation throughout the lungs and trachea. In contrast, in marmosets inoculated via the conventional route, the inflammation was confined to roughly the center of the lung. These data suggest that the tracheal spray route may be more suitable than the conventional route to inoculate marmosets with influenza viruses. We also tested an influenza A(H5N1) highly pathogenic avian influenza (HPAI) virus and found that some marmosets inoculated with this virus via the tracheal spray route showed weight loss, decreased body temperature, and loss of appetite and activity. The replication of this H5N1 virus in respiratory organs was confirmed. These results indicate the potential of marmosets as an animal model for infection with seasonal or HPAI viruses. [ABSTRACT FROM AUTHOR]

Published
2018
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50. Enhanced Replication of Highly Pathogenic Influenza A(H7N9) Virus in Humans.

Author

Seiya Yamayoshi, Maki Kiso, Atsuhiro Yasuhara, Mutsumi Ito, Yuelong Shu, Yoshihiro Kawaoka, Yamayoshi, Seiya, Kiso, Maki, Yasuhara, Atsuhiro, Ito, Mutsumi, Shu, Yuelong, and Kawaoka, Yoshihiro

Subjects
H7N9 Influenza, PATHOGENIC microorganisms, POLYMERASE chain reaction, VIRAL replication, MICROBIAL virulence, INFLUENZA epidemiology, AMINO acids, ANIMAL experimentation, COMPARATIVE studies, GENES, INFLUENZA, RESEARCH methodology, MEDICAL cooperation, MICE, GENETIC mutation, RESEARCH, RESEARCH funding, EVALUATION research, INFLUENZA A virus, ORTHOMYXOVIRUS infections
Abstract

To clarify the threat posed by emergence of highly pathogenic influenza A(H7N9) virus infection among humans, we characterized the viral polymerase complex. Polymerase basic 2-482R, polymerase basic 2-588V, and polymerase acidic-497R individually or additively enhanced virus polymerase activity, indicating that multiple replication-enhancing mutations in 1 isolate may contribute to virulence. [ABSTRACT FROM AUTHOR]

Published
2018
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