Date: Wednesday, 27 October 2021

Venue: Cheung Kung Hai Lecture Theatre 4, G/F, William M.W. Mong Block, Faculty of Medicine Building, 21 Sassoon Road, Pokfulam, Hong Kong

Time: 5:00 p.m. - 6:00 p.m.

5:00 p.m.

Speaker:  Dr. Fatin Nurizzati MOHD JAYA (Post-doctoral Fellow)
Primary Supervisor: Prof. Jiandong HUANG
Presentation Title: The roles of Irx3 and Irx5 in epithelial-neural crest interaction during craniofacial morphogenesis
Abstract: Antigen presentation by the major histocompatibility complex (MHC) molecules is critical for generation of T cell adaptive responses. The large ensemble of peptide presented on the MHC molecules is referred to as the immunopeptidome. Investigating the composition of the immunopeptidome is fundamental to understand the rules that govern antigen presentation and guide the development of next-generation peptide vaccines. Peptide-based vaccination strategies are greatly dependent on the knowledge of epitope presentation, while adjuvants have been traditionally used to enhance the efficacy of such vaccines. It is known that antigen processing machinery is highly regulated by various stimuli, however, the plasticity of presented immunopeptidome repertoire remains largely unknown. In this context, we hope to learn more details on the complexity of peptide presentation by investigating the influence of adjuvants mostly used in therapeutic cancer vaccine and infectious diseases on the naturally processed peptides bound the class I and class II MHC molecules.

5:30 p.m. 

Speaker: Dr. Hinson Pak Hin CHEUNG (Post-doctoral Fellow)
Primary Supervisor: Prof. Dong-Yan JIN
Presentation Title: ORF9b protein of SARS-CoV-2 suppresses MAVS-mediated type I interferon production through MARK3/Par-1a
Abstract: SARS-CoV-2 is the pathogen of COVID-19 that causes over 230 million confirmed cases and nearly 5 million related-deaths. Belonging to the betacoronavirus genus, SARS-CoV-2 expresses lineage-specific accessary proteins shaping its unique pathogenesis. ORF9b is a lineage-specific viral protein conserved among SARS-CoV, SARS-CoV-2 and SARS-like-CoVs. By using BAC carrying SARS-CoV-2 full genome, ORF9b-defective SARS-CoV-2 mutant (Δ9b) was generated. Δ9b was found replicating similarly well as its wild-type counterpart in Vero-E6-hTMPRSS2 cells which were defective to produce type I interferon (IFN), but not in Calu-3 cells which had intact type I IFN antiviral system, suggesting ORF9b can counteract type I IFN production during viral infection. Mechanistically, ORF9b suppressed MAVS-mediated type I IFN production. Through database search of ORF9b interactome, we identified MARK3/Par-1a protein. We found MARK3 not only bound ORF9b but also MAVS protein. MARK3 re-overexpression rescued ORF9b-mediated suppression of MAVS, suggesting that ORF9b suppresses MAVS-mediated type I IFN production through MARK3.

ALL ARE WELCOME

Should you have any enquiries, please feel free to contact Miss River Wong at 3917 9216.