17 results on '"Plianchaisuk A"'
Search Results
2. Virological characteristics of the SARS-CoV-2 Omicron XBB.1.5 variant
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Tomokazu Tamura, Takashi Irie, Sayaka Deguchi, Hisano Yajima, Masumi Tsuda, Hesham Nasser, Keita Mizuma, Arnon Plianchaisuk, Saori Suzuki, Keiya Uriu, Mst Monira Begum, Ryo Shimizu, Michael Jonathan, Rigel Suzuki, Takashi Kondo, Hayato Ito, Akifumi Kamiyama, Kumiko Yoshimatsu, Maya Shofa, Rina Hashimoto, Yuki Anraku, Kanako Terakado Kimura, Shunsuke Kita, Jiei Sasaki, Kaori Sasaki-Tabata, Katsumi Maenaka, Naganori Nao, Lei Wang, Yoshitaka Oda, The Genotype to Phenotype Japan (G2P-Japan) Consortium, Terumasa Ikeda, Akatsuki Saito, Keita Matsuno, Jumpei Ito, Shinya Tanaka, Kei Sato, Takao Hashiguchi, Kazuo Takayama, and Takasuke Fukuhara
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Science - Abstract
Abstract Circulation of SARS-CoV-2 Omicron XBB has resulted in the emergence of XBB.1.5, a new Variant of Interest. Our phylogenetic analysis suggests that XBB.1.5 evolved from XBB.1 by acquiring the S486P spike (S) mutation, subsequent to the acquisition of a nonsense mutation in ORF8. Neutralization assays showed similar abilities of immune escape between XBB.1.5 and XBB.1. We determine the structural basis for the interaction between human ACE2 and the S protein of XBB.1.5, showing similar overall structures between the S proteins of XBB.1 and XBB.1.5. We provide the intrinsic pathogenicity of XBB.1 and XBB.1.5 in hamsters. Importantly, we find that the ORF8 nonsense mutation of XBB.1.5 resulted in impairment of MHC suppression. In vivo experiments using recombinant viruses reveal that the XBB.1.5 mutations are involved with reduced virulence of XBB.1.5. Together, our study identifies the two viral functions defined the difference between XBB.1 and XBB.1.5.
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- 2024
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3. Virological characteristics of a SARS-CoV-2-related bat coronavirus, BANAL-20-236
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Sawa, Hirofumi, Mizuma, Keita, Li, Jingshu, Mimura, Yume, Ohari, Yuma, Tsubo, Tomoya, Ferdous, Zannatul, Shishido, Kenji, Mohri, Hiromi, Iida, Miki, Tsujino, Shuhei, Misawa, Naoko, Usui, Kaoru, Saikruang, Wilaiporn, Lytras, Spyridon, Kawakubo, Shusuke, Nishumura, Luca, Mendoza Tolentino, Jarel Elgin, Li, Wenye, Yo, Maximilian Stanley, Horinaka, Kio, Suganami, Mai, Chiba, Mika, Yoshimura, Ryo, Yasuda, Kyoko, Iida, Keiko, Strange, Adam Patrick, Ohsumi, Naomi, Tanaka, Shiho, Ogawa, Eiko, Okumura, Kaho, Fukuda, Tsuki, Osujo, Rina, Yoshida, Isao, Nakagawa, So, Takaori-Kondo, Akifumi, Shirakawa, Kotaro, Nagata, Kayoko, Nomura, Ryosuke, Horisawa, Yoshihito, Tashiro, Yusuke, Kawai, Yugo, Nakata, Yoshitaka, Futatsusako, Hiroki, Sakamoto, Ayaka, Yasuhara, Naoko, Hashiguchi, Takao, Suzuki, Tateki, Kimura, Kanako, Sasaki, Jiei, Nakajima, Yukari, Yajima, Hisano, Irie, Takashi, Kawabata, Ryoko, Sasaki-Tabata, Kaori, Shimizu, Ryo, Monira Begum, M.S.T., Jonathan, Michael, Mugita, Yuka, Leong, Sharee, Takahashi, Otowa, Ichihara, Kimiko, Ueno, Takamasa, Motozono, Chihiro, Toyoda, Mako, Saito, Akatsuki, Kosaka, Anon, Kawano, Miki, Matsubara, Natsumi, Nishiuchi, Tomoko, Zahradnik, Jiri, Andrikopoulos, Prokopios, Padilla-Blanco, Miguel, Konar, Aditi, Fujita, Shigeru, Plianchaisuk, Arnon, Deguchi, Sayaka, Ito, Hayato, Nao, Naganori, Wang, Lei, Nasser, Hesham, Tamura, Tomokazu, Kimura, Izumi, Kashima, Yukie, Suzuki, Rigel, Suzuki, Saori, Kida, Izumi, Tsuda, Masumi, Oda, Yoshitaka, Hashimoto, Rina, Watanabe, Yukio, Uriu, Keiya, Yamasoba, Daichi, Guo, Ziyi, Hinay, Alfredo A., Jr., Kosugi, Yusuke, Chen, Luo, Pan, Lin, Kaku, Yu, Chu, Hin, Donati, Flora, Temmam, Sarah, Eloit, Marc, Yamamoto, Yuki, Nagamoto, Tetsuharu, Asakura, Hiroyuki, Nagashima, Mami, Sadamasu, Kenji, Yoshimura, Kazuhisa, Suzuki, Yutaka, Ito, Jumpei, Ikeda, Terumasa, Tanaka, Shinya, Matsuno, Keita, Fukuhara, Takasuke, Takayama, Kazuo, and Sato, Kei
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- 2024
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4. Virological characteristics correlating with SARS-CoV-2 spike protein fusogenicity
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MST Monira Begum, Kimiko Ichihara, Otowa Takahashi, Hesham Nasser, Michael Jonathan, Kenzo Tokunaga, Isao Yoshida, Mami Nagashima, Kenji Sadamasu, Kazuhisa Yoshimura, The Genotype to Phenotype Japan (G2P-Japan) Consortium, Kei Sato, Terumasa Ikeda, Keita Matsuno, Naganori Nao, Hirofumi Sawa, Shinya Tanaka, Masumi Tsuda, Lei Wang, Yoshikata Oda, Zannatul Ferdous, Kenji Shishido, Takasuke Fukuhara, Tomokazu Tamura, Rigel Suzuki, Saori Suzuki, Hayato Ito, Jumpei Ito, Yu Kaku, Naoko Misawa, Arnon Plianchaisuk, Ziyi Guo, Alfredo Jr. Hinay, Keiya Uriu, Yusuke Kosugi, Shigeru Fujita, Jarel Elgin Mendoza Tolentino, Luo Chen, Lin Pan, Mai Suganami, Mika Chiba, Ryo Yoshimura, Kyoko Yasuda, Keiko Iida, Naomi Ohsumi, Adam Patrick Strange, Hiroyuki Asakura, So Nakagawa, Akifumi Takaori-Kondo, Kotaro Shirakawa, Kayoko Nagata, Ryosuke Nomura, Yoshihito Horisawa, Yusuke Tashiro, Yugo Kawai, Kazuo Takayama, Rina Hashimoto, Sayaka Deguchi, Yukio Watanabe, Ayaka Sakamoto, Naoko Yasuhara, Takao Hashiguchi, Tateki Suzuki, Kanako Kimura, Jiei Sasaki, Yukari Nakajima, Hisano Yajima, Takashi Irie, Ryoko Kawabata, Kaori Tabata, Ryo Shimizu, Yuka Mugita, Takamasa Ueno, Chihiro Motozono, Mako Toyoda, Akatsuki Saito, Maya Shofa, Yuki Shibatani, and Tomoko Nishiuchi
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SARS-CoV-2 ,fusogenicity ,pathogenicity ,S1/S2 cleavage efficiency ,plaque size ,pseudoviral infectivity ,Microbiology ,QR1-502 - Abstract
IntroductionThe severe acute respiratory syndrome coronavirus (SARS-CoV-2) spike (S) protein is essential in mediating membrane fusion of the virus with the target cells. Several reports demonstrated that SARS-CoV-2 S protein fusogenicity is reportedly closely associated with the intrinsic pathogenicity of the virus determined using hamster models. However, the association between S protein fusogenicity and other virological parameters remains elusive.MethodsIn this study, we investigated the virological parameters (e.g., S1/S2 cleavage efficiency, plaque size, pseudoviral infectivity, pseudovirus entry efficiency, and viral replication kinetics) of eleven previous variants of concern (VOCs) and variants of interest (VOIs) correlating with S protein fusogenicity.Results and discussionS protein fusogenicity was found to be strongly correlated with S1/S2 cleavage efficiency and plaque size formed by clinical isolates. However, S protein fusogenicity was less associated with pseudoviral infectivity, pseudovirus entry efficiency, and viral replication kinetics. Taken together, our results suggest that S1/S2 cleavage efficiency and plaque size could be potential indicators to predict the intrinsic pathogenicity and S protein fusogenicity of newly emerged SARS-CoV-2 variants.
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- 2024
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5. SARS-CoV-2 ORF7a Mutation Found in BF.5 and BF.7 Sublineages Impacts Its Functions
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Uddhav Timilsina, Emily B. Ivey, Sean Duffy, Arnon Plianchaisuk, The Genotype to Phenotype Japan (G2P-Japan) Consortium, Jumpei Ito, Kei Sato, and Spyridon Stavrou
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severe acute respiratory syndrome coronavirus 2 ,open reading frame 7a (ORF7a) ,mutation ,type I interferon response ,major histocompatibility complex I ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
A feature of the SARS-CoV-2 Omicron subvariants BF.5 and BF.7 that recently circulated mainly in China and Japan was the high prevalence of the ORF7a: H47Y mutation, in which the 47th residue of ORF7a has been mutated from a histidine (H) to a tyrosine (Y). Here, we evaluated the effect of this mutation on the three main functions ascribed to the SARS-CoV-2 ORF7a protein. Our findings show that H47Y mutation impairs the ability of SARS-CoV-2 ORF7a to antagonize the type I interferon (IFN-I) response and to downregulate major histocompatibility complex I (MHC-I) cell surface levels, but had no effect in its anti-SERINC5 function. Overall, our results suggest that the H47Y mutation of ORF7a affects important functions of this protein, resulting in changes in virus pathogenesis.
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- 2024
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6. Virological characteristics of a SARS-CoV-2-related bat coronavirus, BANAL-20-236
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Fujita, Shigeru, primary, Plianchaisuk, Arnon, additional, Deguchi, Sayaka, additional, Ito, Hayato, additional, Nao, Naganori, additional, Wang, Lei, additional, Nasser, Hesham, additional, Tamura, Tomokazu, additional, Kimura, Izumi, additional, Kashima, Yukie, additional, Suzuki, Rigel, additional, Suzuki, Saori, additional, Kida, Izumi, additional, Tsuda, Masumi, additional, Oda, Yoshitaka, additional, Hashimoto, Rina, additional, Watanabe, Yukio, additional, Uriu, Keiya, additional, Yamasoba, Daichi, additional, Guo, Ziyi, additional, Hinay, Alfredo A., additional, Kosugi, Yusuke, additional, Chen, Luo, additional, Pan, Lin, additional, Kaku, Yu, additional, Chu, Hin, additional, Donati, Flora, additional, Temmam, Sarah, additional, Eloit, Marc, additional, Yamamoto, Yuki, additional, Nagamoto, Tetsuharu, additional, Asakura, Hiroyuki, additional, Nagashima, Mami, additional, Sadamasu, Kenji, additional, Yoshimura, Kazuhisa, additional, Suzuki, Yutaka, additional, Sawa, Hirofumi, additional, Mizuma, Keita, additional, Li, Jingshu, additional, Mimura, Yume, additional, Ohari, Yuma, additional, Tsubo, Tomoya, additional, Ferdous, Zannatul, additional, Shishido, Kenji, additional, Mohri, Hiromi, additional, Iida, Miki, additional, Tsujino, Shuhei, additional, Misawa, Naoko, additional, Usui, Kaoru, additional, Saikruang, Wilaiporn, additional, Lytras, Spyridon, additional, Kawakubo, Shusuke, additional, Nishumura, Luca, additional, Mendoza Tolentino, Jarel Elgin, additional, Li, Wenye, additional, Yo, Maximilian Stanley, additional, Horinaka, Kio, additional, Suganami, Mai, additional, Chiba, Mika, additional, Yoshimura, Ryo, additional, Yasuda, Kyoko, additional, Iida, Keiko, additional, Strange, Adam Patrick, additional, Ohsumi, Naomi, additional, Tanaka, Shiho, additional, Ogawa, Eiko, additional, Okumura, Kaho, additional, Fukuda, Tsuki, additional, Osujo, Rina, additional, Yoshida, Isao, additional, Nakagawa, So, additional, Takaori-Kondo, Akifumi, additional, Shirakawa, Kotaro, additional, Nagata, Kayoko, additional, Nomura, Ryosuke, additional, Horisawa, Yoshihito, additional, Tashiro, Yusuke, additional, Kawai, Yugo, additional, Nakata, Yoshitaka, additional, Futatsusako, Hiroki, additional, Sakamoto, Ayaka, additional, Yasuhara, Naoko, additional, Hashiguchi, Takao, additional, Suzuki, Tateki, additional, Kimura, Kanako, additional, Sasaki, Jiei, additional, Nakajima, Yukari, additional, Yajima, Hisano, additional, Irie, Takashi, additional, Kawabata, Ryoko, additional, Sasaki-Tabata, Kaori, additional, Shimizu, Ryo, additional, Monira Begum, M.S.T., additional, Jonathan, Michael, additional, Mugita, Yuka, additional, Leong, Sharee, additional, Takahashi, Otowa, additional, Ichihara, Kimiko, additional, Ueno, Takamasa, additional, Motozono, Chihiro, additional, Toyoda, Mako, additional, Saito, Akatsuki, additional, Kosaka, Anon, additional, Kawano, Miki, additional, Matsubara, Natsumi, additional, Nishiuchi, Tomoko, additional, Zahradnik, Jiri, additional, Andrikopoulos, Prokopios, additional, Padilla-Blanco, Miguel, additional, Konar, Aditi, additional, Ito, Jumpei, additional, Ikeda, Terumasa, additional, Tanaka, Shinya, additional, Matsuno, Keita, additional, Fukuhara, Takasuke, additional, Takayama, Kazuo, additional, and Sato, Kei, additional
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- 2024
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7. Virological characteristics of the SARS‐CoV‐2 Omicron EG.5.1 variant.
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Tsujino, Shuhei, Deguchi, Sayaka, Nomai, Tomo, Padilla‐Blanco, Miguel, Plianchaisuk, Arnon, Wang, Lei, Begum, MST Monira, Uriu, Keiya, Mizuma, Keita, Nao, Naganori, Kojima, Isshu, Tsubo, Tomoya, Li, Jingshu, Matsumura, Yasufumi, Nagao, Miki, Oda, Yoshitaka, Tsuda, Masumi, Anraku, Yuki, Kita, Shunsuke, and Yajima, Hisano
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SARS-CoV-2 ,RECOMBINANT viruses ,PATHOGENIC viruses ,SARS-CoV-2 Omicron variant ,ANIMAL culture - Abstract
In middle to late 2023, a sublineage of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) Omicron XBB, EG.5.1 (a progeny of XBB.1.9.2), is spreading rapidly around the world. We performed multiscale investigations, including phylogenetic analysis, epidemic dynamics modeling, infection experiments using pseudoviruses, clinical isolates, and recombinant viruses in cell cultures and experimental animals, and the use of human sera and antiviral compounds, to reveal the virological features of the newly emerging EG.5.1 variant. Our phylogenetic analysis and epidemic dynamics modeling suggested that two hallmark substitutions of EG.5.1, S:F456L and ORF9b:I5T are critical to its increased viral fitness. Experimental investigations on the growth kinetics, sensitivity to clinically available antivirals, fusogenicity, and pathogenicity of EG.5.1 suggested that the virological features of EG.5.1 are comparable to those of XBB.1.5. However, cryo‐electron microscopy revealed structural differences between the spike proteins of EG.5.1 and XBB.1.5. We further assessed the impact of ORF9b:I5T on viral features, but it was almost negligible in our experimental setup. Our multiscale investigations provide knowledge for understanding the evolutionary traits of newly emerging pathogenic viruses, including EG.5.1, in the human population. [ABSTRACT FROM AUTHOR]
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- 2024
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8. Virological characteristics of the SARS-CoV-2 JN.1 variant
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Kaku, Yu, primary, Okumura, Kaho, additional, Padilla-Blanco, Miguel, additional, Kosugi, Yusuke, additional, Uriu, Keiya, additional, Hinay, Alfredo A, additional, Chen, Luo, additional, Plianchaisuk, Arnon, additional, Kobiyama, Kouji, additional, Ishii, Ken J, additional, Zahradnik, Jiri, additional, Ito, Jumpei, additional, and Sato, Kei, additional
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- 2024
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9. SARS-CoV-2 ORF7a Mutation Found in BF.5 and BF.7 Sublineages Impacts Its Functions.
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Timilsina, Uddhav, Ivey, Emily B., Duffy, Sean, Plianchaisuk, Arnon, Ito, Jumpei, Sato, Kei, and Stavrou, Spyridon
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TYPE I interferons ,SARS-CoV-2 ,MAJOR histocompatibility complex - Abstract
A feature of the SARS-CoV-2 Omicron subvariants BF.5 and BF.7 that recently circulated mainly in China and Japan was the high prevalence of the ORF7a: H47Y mutation, in which the 47th residue of ORF7a has been mutated from a histidine (H) to a tyrosine (Y). Here, we evaluated the effect of this mutation on the three main functions ascribed to the SARS-CoV-2 ORF7a protein. Our findings show that H47Y mutation impairs the ability of SARS-CoV-2 ORF7a to antagonize the type I interferon (IFN-I) response and to downregulate major histocompatibility complex I (MHC-I) cell surface levels, but had no effect in its anti-SERINC5 function. Overall, our results suggest that the H47Y mutation of ORF7a affects important functions of this protein, resulting in changes in virus pathogenesis. [ABSTRACT FROM AUTHOR]
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- 2024
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10. Virological characteristics of the SARS-CoV-2 omicron XBB.1.16 variant
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Yamasoba, Daichi, primary, Uriu, Keiya, additional, Plianchaisuk, Arnon, additional, Kosugi, Yusuke, additional, Pan, Lin, additional, Zahradnik, Jiri, additional, Ito, Jumpei, additional, and Sato, Kei, additional
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- 2023
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11. Virological characteristics of the SARS-CoV-2 omicron XBB.1.16 variant
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Daichi Yamasoba, Keiya Uriu, Arnon Plianchaisuk, Yusuke Kosugi, Lin Pan, Jiri Zahradnik, Jumpei Ito, and Kei Sato
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Infectious Diseases - Published
- 2023
12. Origination of LTR Retroelement–Derived NYNRIN Coincides with Therian Placental Emergence
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Arnon Plianchaisuk, Kazuya Kusama, Kiyoko Kato, Sira Sriswasdi, Kazuhiro Tamura, and Wataru Iwasaki
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Mammals ,Genome ,Retroelements ,Pregnancy ,Placenta ,Genetics ,Animals ,Female ,Molecular Biology ,Ecology, Evolution, Behavior and Systematics ,Trophoblasts - Abstract
The emergence of the placenta is a revolutionary event in the evolution of therian mammals, to which some LTR retroelement–derived genes, such as PEG10, RTL1, and syncytin, are known to contribute. However, therian genomes contain many more LTR retroelement–derived genes that may also have contributed to placental evolution. We conducted large-scale evolutionary genomic and transcriptomic analyses to comprehensively search for LTR retroelement–derived genes whose origination coincided with therian placental emergence and that became consistently expressed in therian placentae. We identified NYNRIN as another Ty3/Gypsy LTR retroelement–derived gene likely to contribute to placental emergence in the therian stem lineage. NYNRIN knockdown inhibited the invasion of HTR8/SVneo invasive-type trophoblasts, whereas the knockdown of its nonretroelement-derived homolog KHNYN did not. Functional enrichment analyses suggested that NYNRIN modulates trophoblast invasion by regulating epithelial-mesenchymal transition and extracellular matrix remodeling and that the ubiquitin-proteasome system is responsible for the functional differences between NYNRIN and KHNYN. These findings extend our knowledge of the roles of LTR retroelement–derived genes in the evolution of therian mammals.
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- 2022
13. Origination of LTR Retroelement–Derived NYNRIN Coincides with Therian Placental Emergence
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Plianchaisuk, Arnon, primary, Kusama, Kazuya, additional, Kato, Kiyoko, additional, Sriswasdi, Sira, additional, Tamura, Kazuhiro, additional, and Iwasaki, Wataru, additional
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- 2022
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14. Characteristics of the SARS-CoV-2 omicron HK.3 variant harbouring the FLip substitution
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Misawa, Naoko, Guo, Ziyi, Tolentino, Jarel Elgin M, Fujita, Shigeru, Pan, Lin, Suganami, Mai, Chiba, Mika, Yoshimura, Ryo, Yasuda, Kyoko, Iida, Keiko, Ohsumi, Naomi, Strange, Adam P, Tanaka, Shiho, Fukuhara, Takasuke, Tamura, Tomokazu, Suzuki, Rigel, Suzuki, Saori, Ito, Hayato, Matsuno, Keita, Sawa, Hirofumi, Nao, Naganori, Tanaka, Shinya, Tsuda, Masumi, Wang, Lei, Oda, Yoshikata, Ferdous, Zannatul, Shishido, Kenji, Nakagawa, So, Shirakawa, Kotaro, Takaori-Kondo, Akifumi, Nagata, Kayoko, Nomura, Ryosuke, Horisawa, Yoshihito, Tashiro, Yusuke, Kawai, Yugo, Takayama, Kazuo, Hashimoto, Rina, Deguchi, Sayaka, Watanabe, Yukio, Sakamoto, Ayaka, Yasuhara, Naoko, Hashiguchi, Takao, Suzuki, Tateki, Kimura, Kanako, Sasaki, Jiei, Nakajima, Yukari, Yajima, Hisano, Irie, Takashi, Kawabata, Ryoko, Tabata, Kaori, Ikeda, Terumasa, Nasser, Hesham, Shimizu, Ryo, Begum, MST Monira, Jonathan, Michael, Mugita, Yuka, Takahashi, Otowa, Ichihara, Kimiko, Ueno, Takamasa, Motozono, Chihiro, Toyoda, Mako, Saito, Akatsuki, Shofa, Maya, Shibatani, Yuki, Nishiuchi, Tomoko, Kosugi, Yusuke, Plianchaisuk, Arnon, Putri, Olivia, Uriu, Keiya, Kaku, Yu, Hinay, Alfredo A, Jr, Chen, Luo, Kuramochi, Jin, Sadamasu, Kenji, Yoshimura, Kazuhisa, Asakura, Hiroyuki, Nagashima, Mami, Ito, Jumpei, and Sato, Kei
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- 2024
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15. Multiple mutations of SARS-CoV-2 Omicron BA.2 variant orchestrate its virological characteristics.
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Izumi Kimura, Daichi Yamasoba, Nasser, Hesham, Hayato Ito, Zahradnik, Jiri, Jiaqi Wu, Shigeru Fujita, Keiya Uriu, Jiei Sasaki, Tomokazu Tamura, Rigel Suzuki, Sayaka Deguchi, Arnon Plianchaisuk, Kumiko Yoshimatsu, Yasuhiro Kazuma, Shuya Mitoma, Schreiber, Gideon, Hiroyuki Asakura, Mami Nagashima, and Kenji Sadamasu
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SARS-CoV-2 Omicron variant , *SARS-CoV-2 , *GENETIC mutation , *VIRAL replication - Abstract
Previous studies on the Omicron BA.2 variant suggested that the virological characteristics of BA.2 are determined by the mutations in at least two different regions of the viral genome: in the BA.2 spike gene (enhancing viral fusogenicity and intrinsic pathogenicity) and the non-spike region of the BA.2 genome (leading to intrinsic pathogenicity attenuation). However, the mutations modulating the BA.2 virological properties remain elusive. In this study, we demonstrated that the L371F substitution in the BA.2 spike protein confers greater fusogenicity and intrinsic pathogenicity. Furthermore, we revealed that multiple mutations downstream of the spike gene in the BA.2 genome are responsible for attenuating intrinsic viral pathogenicity and replication capacity. As mutations in the SARS-CoV-2 variant spike proteins could modulate certain virological properties, such as immune evasion and infectivity, most studies have previously focused on spike protein mutations. Our results underpin the importance of non-spike protein-related mutations in SARS-CoV-2 variants. IMPORTANCE Most studies investigating the characteristics of emerging SARS-CoV-2 variants have been focusing on mutations in the spike proteins that affect viral infectivity, fusogenicity, and pathogenicity. However, few studies have addressed how naturally occurring mutations in the non-spike regions of the SARS-CoV-2 genome impact virological properties. In this study, we proved that multiple SARS-CoV-2 Omicron BA.2 mutations, one in the spike protein and another downstream of the spike gene, orchestrally characterize this variant, shedding light on the importance of Omicron BA.2 mutations out of the spike protein. [ABSTRACT FROM AUTHOR]
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- 2023
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16. Characteristics of the SARS-CoV-2 omicron HK.3 variant harbouring the FLip substitution.
- Author
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Kosugi Y, Plianchaisuk A, Putri O, Uriu K, Kaku Y, Hinay AA Jr, Chen L, Kuramochi J, Sadamasu K, Yoshimura K, Asakura H, Nagashima M, Ito J, and Sato K
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- Humans, SARS-CoV-2 genetics, COVID-19
- Abstract
Competing Interests: JI has received consulting fees and honoraria for lectures from Takeda Pharmaceutical. KSat has received consulting fees from Moderna Japan and Takeda Pharmaceutical and has received honoraria for lectures from Gilead Sciences, Moderna Japan, and Shionogi & Co. All other authors declare no competing interests. YKo, AP, and OP contributed equally. This work was supported in part by the Japan Agency for Medical Research and Development (AMED)Strategic Center of Biomedical Advanced Vaccine Research and Development for Preparedness and Response (SCARDA)Japan Initiative for World-leading Vaccine Research and Development Centers UTOPIA (JP223fa627001, to KSat), AMED SCARDA Programme on R&D of New Generation Vaccine including New Modality Application (JP223fa727002, to KSat); AMED Research Programme on Emerging and Re-emerging Infectious Diseases (JP22fk0108146, to KSat; JP21fk0108494, to G2P-Japan Consortium and KSat; JP21fk0108425, to KSat; JP21fk0108432, to KSat; JP22fk0108511, to G2P-Japan Consortium and KSat; JP22fk0108516, to KSat; JP22fk0108506, to KSat); AMED Research Programme on HIV/AIDS (JP22fk0410039, to KSat); JST PRESTO (JPMJPR22R1, to JI); JST CREST (JPMJCR20H4, to KSat); JSPS KAKENHI Grant-in-Aid for Early-Career Scientists (23K14526, to JI); JSPS Core-to-Core Program (A. Advanced Research Networks) (JPJSCCA20190008, to KSat); JSPS Research Fellow DC2 (22J11578, to KU); JSPS Research Fellow DC1 (23KJ0710, to YKo); The Tokyo Biochemical Research Foundation (to KSat); and The Mitsubishi Foundation (to KSat). Members of the G2P-Japan Consortium are listed in the appendix (p 18).
- Published
- 2024
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17. Multiple mutations of SARS-CoV-2 Omicron BA.2 variant orchestrate its virological characteristics.
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Kimura I, Yamasoba D, Nasser H, Ito H, Zahradnik J, Wu J, Fujita S, Uriu K, Sasaki J, Tamura T, Suzuki R, Deguchi S, Plianchaisuk A, Yoshimatsu K, Kazuma Y, Mitoma S, Schreiber G, Asakura H, Nagashima M, Sadamasu K, Yoshimura K, Takaori-Kondo A, Ito J, Shirakawa K, Takayama K, Irie T, Hashiguchi T, Nakagawa S, Fukuhara T, Saito A, Ikeda T, and Sato K
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- Humans, COVID-19 virology, Mutation, SARS-CoV-2 genetics, SARS-CoV-2 pathogenicity, SARS-CoV-2 physiology, Spike Glycoprotein, Coronavirus genetics, Genome, Viral genetics
- Abstract
Importance: Most studies investigating the characteristics of emerging SARS-CoV-2 variants have been focusing on mutations in the spike proteins that affect viral infectivity, fusogenicity, and pathogenicity. However, few studies have addressed how naturally occurring mutations in the non- spike regions of the SARS-CoV-2 genome impact virological properties. In this study, we proved that multiple SARS-CoV-2 Omicron BA.2 mutations, one in the spike protein and another downstream of the spike gene, orchestrally characterize this variant, shedding light on the importance of Omicron BA.2 mutations out of the spike protein., Competing Interests: The authors declare no conflict of interest.
- Published
- 2023
- Full Text
- View/download PDF
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