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Your search keyword '"Huang, Yaoxing"' showing total 9 results
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9 results on '"Huang, Yaoxing"'

1. Author Correction: Identification of SARS-CoV-2 inhibitors using lung and colonic organoids

Author

Han, Yuling, Duan, Xiaohua, Yang, Liuliu, Nilsson-Payant, Benjamin E., Wang, Pengfei, Duan, Fuyu, Tang, Xuming, Yaron, Tomer M., Zhang, Tuo, Uhl, Skyler, Bram, Yaron, Richardson, Chanel, Zhu, Jiajun, Zhao, Zeping, Redmond, David, Houghton, Sean, Nguyen, Duc-Huy T., Xu, Dong, Wang, Xing, Jessurun, Jose, Borczuk, Alain, Huang, Yaoxing, Johnson, Jared L., Liu, Yuru, Xiang, Jenny, Wang, Hui, Cantley, Lewis C., tenOever, Benjamin R., Ho, David D., Pan, Fong Cheng, Evans, Todd, Chen, Huanhuan Joyce, Schwartz, Robert E., and Chen, Shuibing

Published
2024
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5. Developing inhibitory peptides against SARS-CoV-2 envelope protein

Author

Bekdash, Ramsey, primary, Yoshida, Kazushige, additional, Nair, Manoj S., additional, Qiu, Lauren, additional, Ahdout, Johnathan, additional, Tsai, Hsiang-Yi, additional, Uryu, Kunihiro, additional, Soni, Rajesh K., additional, Huang, Yaoxing, additional, Ho, David D., additional, and Yazawa, Masayuki, additional

Published
2024
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6. SARS-CoV-2 infection causes dopaminergic neuron senescence

Author

Yang, Liuliu, Kim, Tae Wan, Han, Yuling, Nair, Manoj S., Harschnitz, Oliver, Zhu, Jiajun, Wang, Pengfei, Koo, So Yeon, Lacko, Lauretta A., Chandar, Vasuretha, Bram, Yaron, Zhang, Tuo, Zhang, Wei, He, Feng, Pan, Chendong, Wu, Junjie, Huang, Yaoxing, Evans, Todd, van der Valk, Paul, Titulaer, Maarten J., Spoor, Jochem K.H., Furler O'Brien, Robert L., Bugiani, Marianna, D.J. Van de Berg, Wilma, Schwartz, Robert E., Ho, David D., Studer, Lorenz, Chen, Shuibing, Yang, Liuliu, Kim, Tae Wan, Han, Yuling, Nair, Manoj S., Harschnitz, Oliver, Zhu, Jiajun, Wang, Pengfei, Koo, So Yeon, Lacko, Lauretta A., Chandar, Vasuretha, Bram, Yaron, Zhang, Tuo, Zhang, Wei, He, Feng, Pan, Chendong, Wu, Junjie, Huang, Yaoxing, Evans, Todd, van der Valk, Paul, Titulaer, Maarten J., Spoor, Jochem K.H., Furler O'Brien, Robert L., Bugiani, Marianna, D.J. Van de Berg, Wilma, Schwartz, Robert E., Ho, David D., Studer, Lorenz, and Chen, Shuibing

Abstract

COVID-19 patients commonly present with signs of central nervous system and/or peripheral nervous system dysfunction. Here, we show that midbrain dopamine (DA) neurons derived from human pluripotent stem cells (hPSCs) are selectively susceptible and permissive to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. SARS-CoV-2 infection of DA neurons triggers an inflammatory and cellular senescence response. High-throughput screening in hPSC-derived DA neurons identified several FDA-approved drugs that can rescue the cellular senescence phenotype by preventing SARS-CoV-2 infection. We also identified the inflammatory and cellular senescence signature and low levels of SARS-CoV-2 transcripts in human substantia nigra tissue of COVID-19 patients. Furthermore, we observed reduced numbers of neuromelanin+ and tyrosine-hydroxylase (TH)+ DA neurons and fibers in a cohort of severe COVID-19 patients. Our findings demonstrate that hPSC-derived DA neurons are susceptible to SARS-CoV-2, identify candidate neuroprotective drugs for COVID-19 patients, and suggest the need for careful, long-term monitoring of neurological problems in COVID-19 patients.

Published
2024

8. SARS-CoV-2 infection causes dopaminergic neuron senescence

Author

Yang, Liuliu, primary, Kim, Tae Wan, additional, Han, Yuling, additional, Nair, Manoj S., additional, Harschnitz, Oliver, additional, Zhu, Jiajun, additional, Wang, Pengfei, additional, Koo, So Yeon, additional, Lacko, Lauretta A., additional, Chandar, Vasuretha, additional, Bram, Yaron, additional, Zhang, Tuo, additional, Zhang, Wei, additional, He, Feng, additional, Pan, Chendong, additional, Wu, Junjie, additional, Huang, Yaoxing, additional, Evans, Todd, additional, van der Valk, Paul, additional, Titulaer, Maarten J., additional, Spoor, Jochem K.H., additional, Furler O’Brien, Robert L., additional, Bugiani, Marianna, additional, D.J. Van de Berg, Wilma, additional, Schwartz, Robert E., additional, Ho, David D., additional, Studer, Lorenz, additional, and Chen, Shuibing, additional

Published
2024
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9. Persistence of an infectious form of SARS-CoV-2 post protease inhibitor treatment of permissive cells in vitro.

Author

Nair MS, Luck MI, Huang Y, Sabo Y, and Ho DD

Abstract

Reports have described SARS-CoV-2 rebound in COVID-19 patients treated with nirmatrelvir, a 3CL protease inhibitor. The cause remains a mystery, although drug resistance, re-infection, and lack of adequate immune responses have been excluded. We now present virologic findings that provide a clue to the cause of viral rebound, which occurs in ∼20% of the treated cases. Persistence of infectious SARS-CoV-2 was experimentally documented in vitro after treatment with nirmatrelvir or another 3CL protease inhibitor, but not with a polymerase inhibitor, remdesivir. This infectious form decayed slowly with a half-life of ∼1 day, suggesting that its persistence could outlive the treatment course to re-ignite SARS-CoV-2 infection as the drug is eliminated. Notably, extending nirmatrelvir treatment beyond 8 days abolished viral rebound in vitro. Our findings point in a particular direction for future investigation of virus persistence and offer a specific treatment recommendation that should be tested clinically., (© The Author(s) 2024. Published by Oxford University Press on behalf of Infectious Diseases Society of America.)

Published
2024
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