刘秀梵团队破解新城疫病毒扩散感染关键机制

Core Insights - The research team led by Academician Liu Xiufan has made significant breakthroughs in understanding the pathogenic mechanism of Newcastle Disease Virus (NDV), as published in the journal PLOS Pathogens [1][2] - The study reveals how NDV utilizes the cytoskeleton to promote its spreading infection, highlighting the molecular mechanisms involved [1][2] Group 1: Research Findings - NDV infection disrupts the expression of tight junction proteins such as OCLN and ZO-1, leading to the breakdown of intercellular tight junction homeostasis, with key roles played by Caspase pathways and viral proteins NP, F, and HN [2] - The research identifies that NDV induces rearrangement of the cytoskeletal protein vimentin and F-actin, forming cage-like structures that enhance viral replication and inflammatory responses through the activation of the MLC/p-MLC pathway [2][3] - This study is the first to elucidate the spreading mechanism of NDV infection and its contribution to systemic tissue damage, providing a new perspective on the disease's pathogenesis [2][3] Group 2: Research Background and Implications - The research originated from observations under a microscope, where it was noted that NDV infection damages tight junction barriers, facilitating the migration and spread of infected cells [3] - Unlike previous studies focused on vaccine prevention, the team explored the virus's own spreading mechanisms, aiming for a more fundamental solution to the problem [3] - The findings explain the molecular basis for the pathogenic differences between strong and weak NDV strains, offering potential targets for vaccine development [3] Group 3: Previous Achievements and Future Directions - Liu Xiufan's team has been dedicated to the epidemiology, prevention, and pathogenic mechanism research of NDV, successfully developing a vaccine that significantly controlled the disease in China [4] - The team has published multiple papers in PLOS Pathogens since 2024, detailing mechanisms of NDV-induced apoptosis in tumor cells and the virus's hijacking of host protein translation systems [4] - These series of studies provide important theoretical support for the design and development of effective oncolytic drugs [4]