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3. Recognition of HIV-1 capsid by PQBP1 licenses an innate immune sensing of nascent HIV-1 DNA

Author

Yoh, Sunnie M., primary, Mamede, João I., additional, Lau, Derrick, additional, Ahn, Narae, additional, Sánchez-Aparicio, Maria T., additional, Temple, Joshua, additional, Tuckwell, Andrew, additional, Fuchs, Nina V., additional, Cianci, Gianguido C., additional, Riva, Laura, additional, Curry, Heather, additional, Yin, Xin, additional, Gambut, Stéphanie, additional, Simons, Lacy M., additional, Hultquist, Judd F., additional, König, Renate, additional, Xiong, Yong, additional, García-Sastre, Adolfo, additional, Böcking, Till, additional, Hope, Thomas J., additional, and Chanda, Sumit K., additional

Published
2022
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4. Sec61 Inhibitor Apratoxin S4 Potently Inhibits SARS-CoV-2 and Exhibits Broad-Spectrum Antiviral Activity

Author

Pohl, Marie O., primary, Martin-Sancho, Laura, additional, Ratnayake, Ranjala, additional, White, Kris M., additional, Riva, Laura, additional, Chen, Qi-Yin, additional, Lieber, Gauthier, additional, Busnadiego, Idoia, additional, Yin, Xin, additional, Lin, Samuel, additional, Pu, Yuan, additional, Pache, Lars, additional, Rosales, Romel, additional, Déjosez, Marion, additional, Qin, Yiren, additional, De Jesus, Paul D., additional, Beall, Anne, additional, Yoh, Sunnie, additional, Hale, Benjamin G., additional, Zwaka, Thomas P., additional, Matsunaga, Naoko, additional, García-Sastre, Adolfo, additional, Stertz, Silke, additional, Chanda, Sumit K., additional, and Luesch, Hendrik, additional

Published
2022
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5. Sec61 Inhibitor Apratoxin S4 Potently Inhibits SARS-CoV-2 and Exhibits Broad-Spectrum Antiviral Activity

Author

Pohl, Marie O; https://orcid.org/0000-0002-9876-3836, Martin-Sancho, Laura, Ratnayake, Ranjala, White, Kris M, Riva, Laura, Chen, Qi-Yin, Lieber, Gauthier; https://orcid.org/0000-0003-0972-6214, Busnadiego, Idoia; https://orcid.org/0000-0002-8781-9099, Yin, Xin, Lin, Samuel; https://orcid.org/0000-0002-4424-7086, Pu, Yuan, Pache, Lars, Rosales, Romel; https://orcid.org/0000-0001-5326-4753, Déjosez, Marion, Qin, Yiren, De Jesus, Paul D, Beall, Anne, Yoh, Sunnie, Hale, Benjamin G; https://orcid.org/0000-0002-3891-9480, Zwaka, Thomas P, Matsunaga, Naoko, García-Sastre, Adolfo; https://orcid.org/0000-0002-6551-1827, Stertz, Silke; https://orcid.org/0000-0001-9491-2892, Chanda, Sumit K, Luesch, Hendrik; https://orcid.org/0000-0002-4091-7492, Pohl, Marie O; https://orcid.org/0000-0002-9876-3836, Martin-Sancho, Laura, Ratnayake, Ranjala, White, Kris M, Riva, Laura, Chen, Qi-Yin, Lieber, Gauthier; https://orcid.org/0000-0003-0972-6214, Busnadiego, Idoia; https://orcid.org/0000-0002-8781-9099, Yin, Xin, Lin, Samuel; https://orcid.org/0000-0002-4424-7086, Pu, Yuan, Pache, Lars, Rosales, Romel; https://orcid.org/0000-0001-5326-4753, Déjosez, Marion, Qin, Yiren, De Jesus, Paul D, Beall, Anne, Yoh, Sunnie, Hale, Benjamin G; https://orcid.org/0000-0002-3891-9480, Zwaka, Thomas P, Matsunaga, Naoko, García-Sastre, Adolfo; https://orcid.org/0000-0002-6551-1827, Stertz, Silke; https://orcid.org/0000-0001-9491-2892, Chanda, Sumit K, and Luesch, Hendrik; https://orcid.org/0000-0002-4091-7492

Abstract

There is a pressing need for host-directed therapeutics that elicit broad-spectrum antiviral activities to potentially address current and future viral pandemics. Apratoxin S4 (Apra S4) is a potent Sec61 inhibitor that prevents cotranslational translocation of secretory proteins into the endoplasmic reticulum (ER), leading to anticancer and antiangiogenic activity both in vitro and in vivo. Since Sec61 has been shown to be an essential host factor for viral proteostasis, we tested Apra S4 in cellular models of viral infection, including SARS-CoV-2, influenza A virus, and flaviviruses (Zika, West Nile, and Dengue virus). Apra S4 inhibited viral replication in a concentration-dependent manner and had high potency particularly against SARS-CoV-2 and influenza A virus, with subnanomolar activity in human cells. Characterization studies focused on SARS-CoV-2 revealed that Apra S4 impacted a post-entry stage of the viral life-cycle. Transmission electron microscopy revealed that Apra S4 blocked formation of stacked double-membrane vesicles, the sites of viral replication. Apra S4 reduced dsRNA formation and prevented viral protein production and trafficking of secretory proteins, especially the spike protein. Given the potent and broad-spectrum activity of Apra S4, further preclinical evaluation of Apra S4 and other Sec61 inhibitors as antivirals is warranted.

Published
2022

6. Sec61 Inhibitor Apratoxin S4 Potently Inhibits SARS-CoV-2 and Exhibits Broad-Spectrum Antiviral Activity

Author

Pohl, Marie O, Martin-Sancho, Laura, Ratnayake, Ranjala, White, Kris M, Riva, Laura, Chen, Qi-Yin, Lieber, Gauthier, Busnadiego, Idoia, Yin, Xin, Lin, Samuel, Pu, Yuan, Pache, Lars, Rosales, Romel, Déjosez, Marion, Qin, Yiren, De Jesus, Paul D, Beall, Anne, Yoh, Sunnie, Hale, Benjamin G, Zwaka, Thomas P, Matsunaga, Naoko, García-Sastre, Adolfo, Stertz, Silke, Chanda, Sumit K, Luesch, Hendrik, University of Zurich, and Luesch, Hendrik

Subjects
10028 Institute of Medical Virology, SARS-CoV-2, Zika Virus Infection, 610 Medicine & health, 2725 Infectious Diseases, Zika Virus, Antiviral Agents, COVID-19 Drug Treatment, Infectious Diseases, Influenza A virus, Depsipeptides, 570 Life sciences, biology, Humans, Pandemics
Abstract

There is a pressing need for host-directed therapeutics that elicit broad-spectrum antiviral activities to potentially address current and future viral pandemics. Apratoxin S4 (Apra S4) is a potent Sec61 inhibitor that prevents cotranslational translocation of secretory proteins into the endoplasmic reticulum (ER), leading to anticancer and antiangiogenic activity both in vitro and in vivo. Since Sec61 has been shown to be an essential host factor for viral proteostasis, we tested Apra S4 in cellular models of viral infection, including SARS-CoV-2, influenza A virus, and flaviviruses (Zika, West Nile, and Dengue virus). Apra S4 inhibited viral replication in a concentration-dependent manner and had high potency particularly against SARS-CoV-2 and influenza A virus, with subnanomolar activity in human cells. Characterization studies focused on SARS-CoV-2 revealed that Apra S4 impacted a post-entry stage of the viral life-cycle. Transmission electron microscopy revealed that Apra S4 blocked formation of stacked double-membrane vesicles, the sites of viral replication. Apra S4 reduced dsRNA formation and prevented viral protein production and trafficking of secretory proteins, especially the spike protein. Given the potent and broad-spectrum activity of Apra S4, further preclinical evaluation of Apra S4 and other Sec61 inhibitors as antivirals is warranted.

Published
2022
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7. Recognition of HIV-1 capsid licenses innate immune response to viral infection

Author

yoh, sunnie M, primary, Mamede, Joao, additional, Lau, Derrick, additional, Ahn, Narae, additional, Sanchez, Maria T, additional, Temple, Joshua, additional, Tuckwell, Andrew, additional, Fuchs, Nina Verena, additional, Cianci, Gianguido, additional, Riva, Laura, additional, Curry, Heather, additional, Yin, Xin, additional, Gambut, Stephanie, additional, Simons, Lacy M., additional, Hultquist, Judd F., additional, Koenig, Renate, additional, Xiong, Yong, additional, Garcia-Sastre, Adolfo, additional, BÖcking, Till, additional, Hope, Thomas J., additional, and Chanda, Sumit, additional

Published
2022
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8. MDA5 Governs the Innate Immune Response to SARS-CoV-2 in Lung Epithelial Cells

Author

Yin, Xin, primary, Riva, Laura, additional, Pu, Yuan, additional, Martin-Sancho, Laura, additional, Kanamune, Jun, additional, Yamamoto, Yuki, additional, Sakai, Kouji, additional, Gotoh, Shimpei, additional, Miorin, Lisa, additional, De Jesus, Paul D., additional, Yang, Chih-Cheng, additional, Herbert, Kristina M., additional, Yoh, Sunnie, additional, Hultquist, Judd F., additional, García-Sastre, Adolfo, additional, and Chanda, Sumit K., additional

Published
2021
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10. MDA5 Governs the Innate Immune Response to SARS-CoV-2 in Lung Epithelial Cells

Author

Yin, Xin, primary, Riva, Laura, additional, Pu, Yuan, additional, Martin-Sancho, Laura, additional, Kanamune, Jun, additional, Yamamoto, Yuki, additional, Sakai, Kouji, additional, Gotoh, Shimpei, additional, Miorin, Lisa, additional, De Jesus, Paul, additional, Yang, Chih-Cheng, additional, Herbert, Kristina, additional, Yoh, Sunnie, additional, Hultquist, Judd, additional, Garcia-Sastre, Adolfo, additional, and Chanda, Summit K., additional

Published
2020
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12. Sensor Sensibility—HIV-1 and the Innate Immune Response.

Author

Xin Yin, Langer, Simon, Zeli Zhang, Herbert, Kristina M., Yoh, Sunnie, König, Renate, and Chanda, Sumit K.

Subjects
IMMUNE response, PATTERN perception receptors, MOLECULAR recognition, NATURAL immunity, HIV, VACCINE effectiveness
Abstract

Innate immunity represents the human immune system’s first line of defense against a pathogenic intruder and is initiated by the recognition of conserved molecular structures known as pathogen-associated molecular patterns (PAMPs) by specialized cellular sensors, called pattern recognition receptors (PRRs). Human immunodeficiency virus type 1 (HIV-1) is a unique human RNA virus that causes acquired immunodeficiency syndrome (AIDS) in infected individuals. During the replication cycle, HIV-1 undergoes reverse transcription of its RNA genome and integrates the resulting DNA into the human genome. Subsequently, transcription of the integrated provirus results in production of new virions and spreading infection of the virus. Throughout the viral replication cycle, numerous nucleic acid derived PAMPs can be recognized by a diverse set of innate immune sensors in infected cells. However, HIV-1 has evolved effcient strategies to evade or counteract this immune surveillance and the downstream responses. Understanding the molecular underpinnings of the concerted actions of the innate immune system, as well as the corresponding viral evasion mechanisms during infection, is critical to understanding HIV-1 transmission and pathogenesis, and may provide important guidance for the design of appropriate adjuvant and vaccine strategies. Here, we summarize current knowledge of the molecular basis for sensing HIV-1 in human cells, including CD4+ T cells, dendritic cells, and macrophages. Furthermore, we discuss the underlying mechanisms by which innate sensing is regulated, and describe the strategies developed by HIV-1 to evade sensing and immune responses. [ABSTRACT FROM AUTHOR]

Published
2020
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15. NLRX1 promotes HIV-1 and DNA viruses replication by blocking STING-TBK1 innate immune signaling

Author

Deng, Meng, primary, Guo, Haitao, additional, König, Renate, additional, Riess, Maximilian, additional, Mo, Jinyao, additional, Zhang, Lu, additional, Petrucelli, Alex, additional, Yoh, Sunnie M., additional, Zhang, Aiping, additional, Colberg-Poley, Anamaris M., additional, Feng, Hui, additional, Lemon, Stanley M., additional, Zhang, Zhigang, additional, Damania, Blossom, additional, Tsao, Li-Chung, additional, Wang, Qi, additional, Su, Lishan, additional, Duncan, Joseph A., additional, Chanda, Sumit K., additional, and Ting, Jenny P, additional

Published
2017
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16. Systems-based analysis of RIG-I-dependent signalling identifies KHSRP as an inhibitor of RIG-I receptor activation

Author

Soonthornvacharin, Stephen, primary, Rodriguez-Frandsen, Ariel, additional, Zhou, Yingyao, additional, Galvez, Felipe, additional, Huffmaster, Nicholas J., additional, Tripathi, Shashank, additional, Balasubramaniam, Vinod R. M. T., additional, Inoue, Atsushi, additional, de Castro, Elisa, additional, Moulton, Hong, additional, Stein, David A., additional, Sánchez-Aparicio, María Teresa, additional, De Jesus, Paul D., additional, Nguyen, Quy, additional, König, Renate, additional, Krogan, Nevan J., additional, García-Sastre, Adolfo, additional, Yoh, Sunnie M., additional, and Chanda, Sumit K., additional

Published
2017
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17. NLRX1 Sequesters STING to Negatively Regulate the Interferon Response, Thereby Facilitating the Replication of HIV-1 and DNA Viruses

Author

Guo, Haitao, primary, König, Renate, additional, Deng, Meng, additional, Riess, Maximilian, additional, Mo, Jinyao, additional, Zhang, Lu, additional, Petrucelli, Alex, additional, Yoh, Sunnie M., additional, Barefoot, Brice, additional, Samo, Melissa, additional, Sempowski, Gregory D., additional, Zhang, Aiping, additional, Colberg-Poley, Anamaris M., additional, Feng, Hui, additional, Lemon, Stanley M., additional, Liu, Yong, additional, Zhang, Yanping, additional, Wen, Haitao, additional, Zhang, Zhigang, additional, Damania, Blossom, additional, Tsao, Li-Chung, additional, Wang, Qi, additional, Su, Lishan, additional, Duncan, Joseph A., additional, Chanda, Sumit K., additional, and Ting, Jenny P.-Y., additional

Published
2016
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18. PQBP1 Is a Proximal Sensor of the cGAS-Dependent Innate Response to HIV-1

Author

Yoh, Sunnie M., primary, Schneider, Monika, additional, Seifried, Janna, additional, Soonthornvacharin, Stephen, additional, Akleh, Rana E., additional, Olivieri, Kevin C., additional, De Jesus, Paul D., additional, Ruan, Chunhai, additional, de Castro, Elisa, additional, Ruiz, Pedro A., additional, Germanaud, David, additional, des Portes, Vincent, additional, García-Sastre, Adolfo, additional, König, Renate, additional, and Chanda, Sumit K., additional

Published
2015
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23. Molecular Analysis of Human Resistance to Thyroid Hormone Syndrome.

Author

Walker, John M., Baniahmad, Aria, Yoh, Sunnie M., and Privalsky, Martin L.

Abstract

Resistance to thyroid hormone (RTH) syndrome is an inherited human endocrine disease, which is manifested as a failure to respond properly to elevated circulating thyroid hormone (1-4). RTH syndrome behaves as an autosomal dominant trait, and has been mapped at the molecular level to a diverse array of mutations within the thyroid hormone receptor (TR)-β locus (1-4). As detailed elsewhere in this review series, TRs bind to specific DNA sequences, denoted thyroid hormone response elements (TREs) and regulate transcription of adjacent target genes in response to thyroid hormone (5-7). TRs typically repress transcription in the absence of hormone and activate transcription in the presence of hormone (8-10). These bipolar transcriptional properties of the receptor are mediated by the receptor's ability to recruit ancillary polypeptides, denoted corepressors and coactivators, to the target promoter (11-16). Corepressors and coactivators modulate transcription both by covalent modification of the chromatin template and by direct interactions with components of the general transcriptional machinery. Corepressors are typically recruited by TRs in the absence of hormone, whereas binding of hormone to the TRs results in a release of the corepressors and a recruitment of the coactivator polypeptides (11-16). [ABSTRACT FROM AUTHOR]

Published
2002
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