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Alistair Russell

Research

Nearly every cell in the human body has the capacity to respond to a viral infection with the production of interferons—critical components of cell intrinsic immunity that drive resolution of disease, and, unfortunately, much of the resultant immunopathology. Unsurprisingly, viruses circumvent, co-opt, or otherwise subvert the induction of an antiviral state. Regardless, no defense (or offense) is perfect, and viral populations almost invariably induce interferon in a small fraction of infected cells. Some of this rarity of response is driven by rare viral failure to suppress interferon, in part due to the extreme variation evinced by many viral populations. However, the rarity of response is also partially explained by intrinsic host mechanisms suppressing spurious activation—seeking to avoid the resultant cost from an overly sensitive triggering of inflammatory processes.

My lab seeks to study the rarity of the interferon response during viral infection using influenza A virus as a model, using single-cell transcriptomics, single virion genomics, flow cytometry, population-based sequencing, and fine-grained genetic analyses to delineate the molecular events that proceed engagement of innate immune signaling pathways in responding cells. With these data in hand, we will seek to better model disease processes, with the hope that our work may help development of therapeutic interventions or more robust vaccine responses.

Select Publications

  • Mendes M, Russell AB (2021) Library-based analysis reveals segment and length dependent characteristics of defective influenza genomes. PLoS Pathog 17(12): e1010125. https://doi.org/10.1371/journal.ppat.1010125
  • Russell, A.B., Elshina, E., Kowalsky, J.R., te Velthuis, A.J., Bloom, J.D., (2019) Single-cell virus sequencing of influenza infections that trigger innate immunity. Journal of Virology. 0022-538X
  • Russell, A.B., Trapnell, C., Bloom, Bloom, J.D., (2018) Extreme heterogeneity of influenza virus infection in single cells. eLife. 7, e02020
  • Russell, A.B., Wexler, A.G., Brittany, H.N., Whitney, J.C., Bohn, A.J., Young Ah, G., Tran, B.Q., Natasha, B., Zheng, H., Peterson, S.B., Chou, S., Gonen, T., Goodlett, D.R., Goodman, A.L., Mougous, J.D. (2014) A type VI secretion-related pathway in Bacteroidetes mediates interbacterial antagonism. Cell Host and Microbe. 16, 227-236
  • Russell, A.B., Peterson, S.B., Mougous, J.D. (2014) Type VI secretion effectors: poisons with a purpose. Nature Reviews Microbiology. 12, 137-148
  • Russell, A.B., LeRoux, M., Hathazi, K., Agnello, D.M., Ishikawa, T., Wiggins, P.A., Wai, S.W., Mougous, J.D. (2013) Diverse type VI secretion phospholipases are functionally plastic antibacterial effectors. Nature. 496, 508-512
  • Russell, A.B.*, Singh, P.*, Brittnacher, M., Bui, N.K., Hood, R.D., Carl, M.A., Agnello, D.M., Schwarz, S., Goodlett, D.R., Vollmer, W., and Mougous, J.D. (2012) A widespread bacterial type VI secretion effector superfamily identified using a heuristic approach. Cell Host and Microbe. 11, 538-549
  • Russell, A.B., Hood, R.D., Bui, N.K., LeRoux, M., Vollmer, W. and Mougous, J.D. (2011) Type VI secretion delivers lytic effectors to the periplasm of target cells. Nature. 475, 343-347
  • Munkvold, K.R.*, Russell, A.B.*, Kvitko, B.H., and Collmer, A.R. (2009) Pseudomonas syringae pv. tomato DC3000 type III effector HopAA1-1 functions redundantly with chlorosis-promoting factor PSPTO4723 to produce bacterial speck lesions in host tomato. Molecular Plant Microbe Interactions. 22, 1341-1355
  • Wexler, A.G., Bao, Y., Whitney, J.C., Bobay, L.M., Xavier, J.B., Schofield, W.B., Barry, N.A., Russell, A.B., Tran, B.Q., Goo, Y.A., Goodleyy, D.R., Ochman, H., Mougous, J.D., Goodman, A.L. (2016) Human symbionts inject and neutralize antibacterial toxins to persist in the gut. Proceedings of the National Academy of Sciences. 113, 3639-3644
  • LeRoux, M., Kirkpatric, R.L., Montauti, E.I., Tran, B.Q., Peterson, S.B., Harding, B.N., Whitney, J.C., Russell, A.B., Traxler, B., Goo, Y.A., Goodlett, D.R., Wiggins, P.A., Mougous, J.D. (2015) Kin cell lysis is a danger signal that activates antibacterial pathways of Pseudomonas aeruginosa. eLife. 4, e05701
  • Whitney, J.C., Beck, C.M., Goo, Y.A., Russell, A.B., Harding, B., De Leon, J.A., Cunningham, D.A., Tran, B.Q., Low, D.A., Hayes, C.S., Mougous, J.D. (2014) Genetically distinct pathways guide effector export through the type VI secretion system. Molecular Microbiology. 92, 529-542

Biography

Alistair Russell received his PhD from the University of Washington in the laboratory of Joseph Mougous, where, supported by the NSF, he studied interbacterial interactions driven by the type VI secretion system, using a combination of genetic, informatic, and biochemical tools. For his postdoctoral research, he worked as a Merck Fellow of the Damon Runyon Cancer Research Foundation, in the laboratory of Jesse Bloom at the Fred Hutchinson Cancer Research Center, trying to use novel single-cell methodologies to unravel events precipitating induction of an interferon response by influenza A virus. He joined the Molecular Biology faculty at UCSD in 2019.

Alistair Russell