Role of Rab11 in Influenza B Virus Infection
Fanuele, Conor
Fanuele, Conor
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Abstract
Influenza virus poses a threat to public health with seasonal flu causing 3-5 million cases of severe illness annually. While �seasonal flu� includes both Influenza A virus (IAV) and Influenza B virus (IBV), most research focuses on IAV. Yet, in recent years IBV contributed to 16-52% of influenza-associated pediatric deaths in the US. Influenza is an obligate intracellular pathogen, requiring both IAV and IBV to co-opt host trafficking machinery during the life cycle. Rab11 is a cellular GTPase that traffics cargo to and from the plasma membrane, and prior research has shown that IAV utilizes the Rab11 pathway during viral infection to transport the viral genome segments to the site of budding. While IAV and IBV share a reasonable degree of sequence homology, there is a critical gap in knowledge regarding how IBV completes viral assembly, and whether it also requires the cellular Rab11 pathway. We investigated whether Rab11 is required during IBV infection by using siRNA to deplete specific Rab proteins in human airway epithelial (A549) cells. Depletion of both Rab11A and Rab11B individually showed significant decrease in viral titer and nucleoprotein (NP) expression in infected cells. This data indicates that IBV is likely to also require Rab11 during infection. Decreased viral protein expression could indicate that, unlike specific strains of IAV, IBV utilizes Rab11 at an earlier point in the viral lifecycle prior to trafficking vRNPs. Defects in protein production could alternatively be caused by compounding effects on viral release, decreasing the efficiency of a second round of viral infection. Our next steps will address the role of Rab11 in IBV infection, including the stage of the viral life cycle that Rab11 is contributing to.
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Date
1/1/2026
Student Status
Senior (Graduating in 2026)
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Oral Presentation
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Microbiology
College/School
College of Agriculture and Life Sciences
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Life Science