Abstract The induction of broadly neutralizing antibodies (bnAbs) against viruses requires the specific activation of human B cell receptors (BCRs) by viral epitopes. Following BCR activation, B cells can undergo germinal center–dependent and –independent pathways to generate both long-term and short-term epitope-specific memory responses. However, the regulation of B cell fate after BCR activation remains incompletely understood. Here, the speaker will report that a human isoform of PD-1, namely Δ42PD-1, plays a critical role in regulating B cell fate following BCR activation. While HIV-1 promotes B cell apoptosis via the epitope–BCR–Δ42PD-1 axis during chronic infection, SARS-CoV-2 does not appear to activate this pathway after breakthrough infections. This allows for more robust induction of bnAbs by engaging multiple highly conserved conformational “Jing” epitopes, as revealed by CryoEM analysis. “Jing” follows the Chinese philosophy: “unchanging principles are the best response to change”. Consequently, bnAbs are induced not only against a broad range of evolving SARS-CoV-2 variants but also against pan-sarbecoviruses, including SARS-CoV-1 and SARS-CoV-2 variants, as well as related pangolin-CoV and bat-CoV strains. These findings have important implications for understanding human B cell immunity and for the design of novel vaccines against pan-sarbecoviruses. About the Speaker Prof. CHEN Zhiwei received his PhD from the New York University School of Medicine in 1996 and, by 2002, had progressed from an NIH F32 Postdoctoral Fellow to Assistant Professor at the Aaron Diamond AIDS Research Center of The Rockefeller University. In 2007, he joined the Li Ka Shing Faculty of Medicine of the University of Hong Kong (HKU) as an Associate Professor and Founding Director of the AIDS Institute. He is a former Chairman of the Hong Kong Society for Immunology and an Executive Committee Member of the China AIDS Vaccine Initiative. He also served as a Member of the Hong Kong Advisory Council on AIDS for the HKSAR Department of Health from 2008 to 2014. He is currently a Chair Professor of Immunology and Immunotherapy in the Department of Microbiology at HKU. He was conferred the Suen Chi-Sun Professorship in Clinical Science in 2024. Prof. Chen’s research focuses on AIDS, SARS and COVID-19 pathogenesis and immunotherapy, with an emphasis on the early events of viral infection. He pioneered the creation of HKU-patented platforms of technologies, including the PD1-based vaccine, the tandem anti-HIV-1 bi-specific antibody, and an anti-Δ42PD1 antibody drug for viral infection and cancer. Clarivate Analytics has ranked him among the top 1% of researchers worldwide by citations and a Highly Cited Researcher in 2022, 2023 and 2024. He has won numerous research grants as PI from, for example, NIH RO1, amfAR and the Gates Foundation among others. He also won the HKU Knowledge Exchange Excellence Award (2019), Outstanding Researcher Award (2021), Outstanding Research Student Supervisor Award (2021) and Faculty Outstanding Research Output Award (2023). For Attendees' Attention Seating is on a first come, first served basis.

Abstract Genetically modified animal models have been extensively used to investigate the pathogenesis of age-dependent neurodegenerative diseases, such as Alzheimer (AD), Parkinson (PD), Huntington (HD) diseases, and Amyotrophic Lateral Sclerosis (ALS). The common feature of these diseases is the age-dependent accumulation of misfolded proteins in the brain, which can be recapitulated in a variety of mouse models of neurodegenerative diseases. However, the brains of transgenic mouse models of AD, PD, and HD do not show the striking neuronal loss or degeneration that is a typical pathological feature in patient brains. Species differences between small animals and humans may account for differential pathology in transgenic mouse models and patient brains. Using CRISPR/Cas9 to modify the endogenous disease genes in large animals (pigs and monkeys), the speaker and his research team demonstrate that typical neuropathological features can be mimicked in the brains of large animals.  The findings underscore the importance of using large mammals to investigate the pathogenesis of important brain diseases and their therapeutics. About the Speaker Prof. LI Xiao-Jiang is a Professor at Jinan University. He also serves as the Director of the Guangdong Key Laboratory of Non-human Primate Research. Prof. Li obtained his PhD from Oregon Health & Science University and completed his postdoctoral training at Johns Hopkins University in the US. From 1996 to 2019, he worked in the Department of Human Genetics at Emory University, where he was promoted to tenured full professor in 2005 and has held the title of Distinguished Professor since 2007. Between 2012 and 2016, he conducted research at the Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, where he utilized CRISPR/Cas9 technology to establish large animal models of human diseases. In 2019, he joined Jinan University on a full-time basis and currently holds a professorship at the Guangdong-Hong Kong-Macau Institute of CNS Regeneration at Jinan University. Prof. Li is dedicated to studying early nervous system development, aging, and neurodegenerative diseases, employing transgenic disease animal models such as mice, pigs, and monkeys. He is currently focused on elucidating pathogenic mechanisms using genetically modified large animal models. His research findings have been published in over 250 international journals, including reputable publications like Cell and Nature, with cumulative citations exceeding 33,810 and an H-index of 95. . For Attendees' Attention Seating is on a first come, first served basis.  

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