William T. Jackson, PhD

K. Kirkegaard, M. Taylor, and W.T. Jackson. Cellular autophagy: surrender, avoidance and subversion by microorganisms. Nat Rev Microbiol. 2004 Apr;2(4):301-314. (Review)

W.T. Jackson, T.H. Giddings, M.P. Taylor, S. Mulinyawe, M. Rabinovitch, R.R. Kopito , K. Kirkegaard. Subversion of cellular autophagosomal machinery by RNA viruses. PLoS Biol. 2005 May;3(5) PMCID: PMC1084330

K. Kirkegaard and W.T.Jackson, Topology of Double-Membraned Vesicles and the Opportunity for Non-Lytic Release of Cytoplasm. Autophagy 2005 Oct 1(3):182-4. (Review)

W.T. Jackson and G.S. Martin. Transcription of the Schizosaccharomyces pombe gene cdc18⁺: roles of MCB elements and the DSC1 complex. Gene 2006 Mar. 15, 369: 100-108.

D. Klionsky, et.al. Guidelines for Monitoring Autophagy in Higher Eukaryotes. Autophagy 2008 Mar- Apr;4(2):151-75.

M.P. Taylor, T. B. Burgon, K. Kirkegaard and W.T. Jackson. Role of microtubules in extracellular release of poliovirus. J. Virology 2009 Jul; 83(13):6599-609. PMCID: PMC2698579

P. Parameswaran, E. Sklan, C. Wilkins, T. Burgon, M.A. Samuel, R. Lu, K.M. Ansel, V. Heissmeyer, S. Einav, W.T. Jackson, T. Doukas, S. Paranjape, C. Polacek, F.B. Dos Santos, R. Jalili, F. Babrzadeh, B. Gharizadeh, D. Grimm, M. Kay, S. Koike, P. Sarnow, M. Ronaghi, S.W. Ding, E. Harris, M. Chow, M.S. Diamond, K. Kirkegaard, J.S. Glenn and A.Z. Fire. Six RNA Viruses and Forty-One Hosts: Viral Small RNAs and Modulation of Small RNA Repertoires in Vertebrate and Invertebrate Systems. PLoS Pathogens 2010 Feb;6(2). PMCID: PMC2820531

V. O'Donnell, J.M. Pacheco, M. Larocco, T. Burrage, W.T. Jackson, L.L.Rodriguez, M.V. Borca, and  B. Baxt. Foot-and-mouth disease virus utilizes an autophagic pathway during viral replication. Virology. 2011 Feb 5;410(1):142-50. PMCID: PMC21112602

K.A. Klein and W.T. Jackson. Human rhinovirus 2 induces the autophagic pathway and replicates more efficiently in autophagic cells. J. Virology 2011 Sep;85(18):9651-4. PMCID: PMC3165776

K.A. Klein and W.T. Jackson. Picornavirus subversion of the autophagy pathway. Viruses 2011 Sep;3(9):1549-61. (Review) PMCID: PMC3187694

D. Klionsky, et.al. Guidelines for Monitoring Autophagy in Higher Eukaryotes. Autophagy 2012  Apr;8(4):445-544. PMCID: PMC3404883

A.L. Richards and W.T. Jackson. That which does not degrade you makes you stronger: Infectivity of poliovirus depends on vesicle acidification. Autophagy 2013 May;9(5) (Review) PMCID: PMC3669197

A.L. Richards and W.T. Jackson. Behind closed membranes: the secret lives of picornaviruses? PLoS Pathogens, 2013 May;9(5). (Opinion) PMCID: PMC3642085

A.L. Richards and W.T. Jackson. How positive-strand RNA viruses benefit from autophagosome maturation.” J Virol.2013 Sep;87(18):9966-72. (Review) PMCID: PMC3754026

J.S. Tam, W.T. Jackson, D. Hunter, D. Proud, and M.H. Grayson. Rhinovirus specific IgE can be detected in human sera. J Allergy Clin Immunol. 2013 Nov;132(5)

W.T. Jackson. Autophagy as a broad antiviral at the placental interface. (Editor’s Corner.) Autophagy. 2013 Dec;9(12):1905-7

A.L. Richards, J.A.P. Soares-Martins, G.T. Riddell, and W.T. Jackson. Generation of unique poliovirus RNA replication organelles. MBio 2014, 5. PMCID:PMC3940031

W.T. Jackson. Poliovirus-induced changes in cellular membranes throughout infection. Current Opinion in Virology, 2014, 9:67–73. PMCID:PMC4267968

Delorme-Axford E, Morosky S, Bomberger J, Stolz DB, W.T. Jackson, Coyne CB. BPIFB3 regulates autophagy and coxsackievirus B replication through a noncanonical pathway independent of the core initiation machinery. mBio 2014 5(6):e02147-14. PMCID:PMC4324245

W.T. Jackson. Viruses and the autophagy pathway. Virology. 2015 May;479-480:450-6

When a picornavirus moves into a cell, it does so with the goal of turning the cell into a virus factory. Most of the normal functions of a cell are shut down and the cell's resources are diverted to the service of the virus. Most dramatically, the cell's innards are rearranged to the point that they become irreversibly damaged and unrecognizable. The virus uses the rearranged cell membranes to set up genetic "copying centers" where the genetic material of the virus is replicated. Our lab studies the large variety of tricks employed by these viruses to rearrange cell membranes.

For example, poliovirus triggers a "starvation response" so that the cell generates double-membraned structures called autophagosomes. Autophagosomes typically act as recycling centers, gathering up cellular contents and chewing them up so the starving cell has the raw materials to build new proteins. Poliovirus, however, uses these recycling centers produce infectious virus particles.

We have found that some common cold viruses use this same strategy. However, we also found that one particular common cold virus, Rhinovirus 1A, uses a different trick. It causes the Golgi apparatus, which is used by the cells to sort newly made proteins, to break up into round "vesicles" which provide a base for virus genome factories.

We also study the emerging pathogen Enterovirus D-68 (EVD-68), a respiratory pathogen of chidren which may be associated with acute flaccid myelitis and Guillain-Barré syndrome. Our previous work on poliovirus and rhinovirus has allowed us to quickly assess the intracellular life cycle of this under-studied virus. EVD-68 also induces autophagosomes and regulates this cellular pathway in novel ways.

What's surprising is that, to a virologist, poliovirus, EVD-68, and Rhinovirus 1A are close cousins, and both need to rearrange cell membranes to produce progeny viruses. However, each regulates cellular membrane formation in a unique way. How do each of their strategies work? Is there some common element among these viruses we could use to target therapeutics and eventually develop a cure for EVD-68, CVB3, and the common cold? These questions currently drive our research.