Huerta, Carlos Theodore2016-06-062016-06-062015-05http://hdl.handle.net/10267/27450Permission to publish this honors paper was granted by the author and submitted on a CD.Highly pathogenic H5N1 influenza virus infections are associated with severe respiratory damage and high morbidity and mortality in infected humans. Due to the critical role that macrophages play in response to respiratory pathogens, investigating such viruses’ ability to evade or exploit the innate immune response can provide greater insight into macrophage function at the host-pathogen interface. Unlike H5 viruses, we found that all non-H5 influenza virus strains including the 2009 H1N1 pandemic virus experience a block upstream of nuclear entry and escape and are unable to replicate in macrophages. However, only highly pathogenic H5N1 strains could successfully produce new viral protein synthesis and progeny release. Furthermore, it was found that the pH of fusion of the hemagglutinin (HA) protein, not sialic acid receptor binding, influenced replication. On a functional level, it was shown that while reactive oxygen species (ROS) were not produced during viral infection, macrophage phagocytosis was significantly impaired by productive viral replication. Future studies will focus on elucidating the molecular mechanism(s) of these blocks in differential H5 virus-specific replication, and the overall effect of viral replication in in vivo model systems.Rhodes College owns the rights to the archival digital objects in this repository. Objects are made available for educational use only and may not be used for any non-educational or commercial purpose. Approved educational uses include private research and scholarship, teaching, and student projects. Original copies of the minutes are stored in the CollegeBiology, Department ofHonors papersStudent researchThesis