Identifying how airway immune cells block respiratory virus replication
Alveolar macrophages are susceptible to seasonal IAV infection but block virus growth whereas monocyte-derived macrophages and airway epithelial cells support virus growth. Therefore, alveolar macrophages express (unknown) host factors that block seasonal IAV. Of interest, highly pathogenic avian influenza (HPAI) H5N1 does grow in alveolar macrophages and therefore evades restriction factors that block seasonal IAV. In Sarah’s laboratory, they have established experimental in vitro approaches to identify cellular factors that block the growth of seasonal IAV. Moreover, they are investigating determinants of HPAI H5N1 infection that allow these viruses to evade restriction by specific cellular factors. Sarah’s group is also investigating how airway immune cells respond to infection with other respiratory viruses, including SARS-CoV-2. These in vitro approaches are complemented through use of primary cells isolated from patients at the Royal Melbourne Hospital.
Dr Sarah Londrigan
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Dr Sarah Londrigan is a teaching and research academic in the Department of Microbiology and Immunology at the University of Melbourne, leading a program examining cellular responses to respiratory virus infection. She is a lead for the Viral Infectious Diseases at the Doherty Institute. She completed her undergraduate and PhD studies at the University of Melbourne, where she identified novel cell surface receptors for rotavirus. Sarah’s postdoctoral research at the Walter and Eliza Hall Institute (WEHI) involved creating immunomodulatory adenoviruses that generated local immunosuppression during islet transplantation to treat Type I diabetes. Since 2008, her research has focused on pathways that influenza, and other respiratory viruses, use to infect host cells. Current projects include investigating why particular respiratory viruses are highly pathogenic, leading to very severe disease.