Wang lab


Cell biology of viral infections


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our research



Virus infection is a dynamic process and highly dependent on the host cells. Our laboratory endeavor to understand how viruses exploit cellular machineries, such as to achieve their infection and replication. Our research focuses on the late stages of influenza virus life cycle, including virion assembly, egress and transmission between cells. These critical steps enable the genome reassortment, guarantee the formation of infective progeny virions, and release them from the host to establish new infections. We aim to elucidate the virus-host interaction in these infection steps, its kinetics, and the underlying regulatory mechanisms. To resolve the dynamic and complex infection processes, we employ an interdisciplinary approach leveraging tools from molecular virology, cell biology, advanced light/EM microscopy, and computational analyses. We hope that our research will yield new insights into the cell biology of virus infection, and thereby provide a basis for the development of future therapeutics against influenza.



Mechanism of viral genome packaging



The genome of influenza virus comprises eight segments of negative-strand RNA. Upon egress, progeny virions have to correctly "pack" each of all 8 viral RNA segments to ensure their infectivity. We are studying how influenza virus achieves this selective packaging and delivers its assembled genome to the cell membrane for the subsequent budding.



Virus egress with cytoskeleton



Viruses require the assistance from the host cells to cause an infection and transfer viral genes into host cells. As many cellular processes directly or indirectly depend on cytoskeleton, we have a continuing interest in the virus-cytoskeleton interaction upon infection. We are now investigating the temporal and spatial regulation of the interaction between viral genome and actin, and how influenza virus mediates actin filament homeostasis upon the egress for its own benefit.



© I-Hsuan Jessica Wang