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John S. L. Parker, BVMS, Ph.D.

Associate Professor of Virology

Dr. John Parker studies viruses and the ways in which animals respond to viral infection, laying the basic science groundwork for ways to improve diagnosis, treatment, and prevention of these diseases. His lab is focused on viruses that infect humans and animals, including reovirus and feline calicivirus, and the results of most of his projects can be broadly applied to benefit the health of animals and humans alike.

Reoviruses infect a broad range of different species, including humans, dogs, cats, and many others. Although these infections are very common, particularly among children and younger animals, reovirus infections are usually mild and symptoms are minimal. Though not especially threatening in and of themselves, reoviruses are good representatives for the ways other, more virulent and severe viruses work, so Dr. Parker and his colleagues use reovirus infection as a model system for understanding virus biology. They’re investigating how reovirus exploits the host’s resources to replicate itself, and they’re developing new models to explain the steps a virus takes to translate its genetic material into proteins. Knowing how reovirus accomplishes replication could lead to methods for inhibiting that process and shutting down infections.

The Parker lab is also studying the ways in which another common pathogen, feline calicivirus, evades the immune system. Feline calicivirus often causes upper respiratory tract infections – commonly called “cat flu” – but more virulent strains of the virus can cause severe pneumonia, liver necrosis, pancreatitis, and other complications. Infection with these more virulent strains is fatal for 50-60% of cats. Dr. Parker and his colleagues are investigating the differences between the less virulent and highly virulent strains of calicivirus that might explain these varying effects. Feline calicivirus is closely related to human norovirus, a highly infectious pathogen notorious for causing widespread outbreaks of gastrointestinal illness, but since norovirus is difficult to study in the lab, much about this common human pathogen remains a mystery. Studies of feline calicivirus strains and the ability of the host to neutralize these viruses can offer valuable insights that not only save cats, but may also help guide efforts to bolster the human immune response to norovirus.

Pathogenic viruses like calicivirus and norovirus cause incredible mortality and suffering among animals and humans, powerful effects that belie their relative smallness and genetic limitations. Recent studies show that cytomegalovirus produces more protein products than would be predicted from its small number of genes, a finding that helps to explain how the virus is capable of achieving a great complexity of interactions and effects from seemingly meager genetic tools. Dr. Parker’s lab is tallying the protein products of such viruses as herpes simplex virus, influenza, and reovirus during infection to determine whether this phenomenon applies to other kinds of viruses. Aside from the interest to basic biology, the results will also help to identify whether there are a core set of proteins that all viruses employ during infection, a sort of common arsenal shared among viruses of many types. If so, those proteins might be used as an indicator to diagnose viral infections of many kinds, even infections caused by emerging viruses that haven’t been thoroughly characterized in the lab, an increasing common public health concern.


Publications:

1.  Connelly JT, Kondapalli S, Skoupi M, Parker JS, Kirby BJ, Baeumner AJ. (2012). Micro-total analysis system for virus detection: microfluidic pre-concentration coupled to liposome-based detection. Analytical and Bioanalytical Chemistry, 402(1):315-23. Abstract.

2.  Pesavento P1, Liu H, Ossiboff RJ, Stucker KM, Heymer A, Millon L, Wood J, van der List D, Parker JS. (2009). Characterization of a continuous feline mammary epithelial cell line susceptible to feline epitheliotropic viruses. Journal of Virological Methods, 157(1):105-10. Abstract.

3.  Pesavento PA1, Chang KO, Parker JS. Molecular virology of feline calicivirus. Veterinary Clinics of North America – Small Animal Practice, 38(4):775-86, vii. Abstract.

5.  Ossiboff RJ1, Sheh A, Shotton J, Pesavento PA, Parker JS. (2007). Feline caliciviruses (FCVs) isolated from cats with virulent systemic disease possess in vitro phenotypes distinct from those of other FCV isolates. Journal of General Virology, 88(Pt 2):506-17. Abstract.

6.  Kaufer S1, Coffey CM, Parker JS. (2012). The cellular chaperone hsc70 is specifically recruited to reovirus viral factories independently of its chaperone function. Journal of Virology, 86(2):1079-89.

7.  Kim JW1, Lyi SM, Parrish CR, Parker JS. (2011). A proapoptotic peptide derived from reovirus outer capsid protein {micro}1 has membrane-destabilizing activity. Journal of Virology, 85(4):1507-16.

8.  Coffey CM, Sheh A, Kim IS, Chandran K, Nibert ML, Parker JS. (2011). Reovirus Outer Capsid Protein μ1 Induces Apoptosis and Associates with Lipid Droplets, Endoplasmic Reticulum, and Mitochondria. Journal of Virology, 80(17): 8422–8438.

9.  Ossiboff RJ1, Zhou Y, Lightfoot PJ, Prasad BV, Parker JS. Conformational changes in the capsid of a calicivirus upon interaction with its functional receptor. Journal of Virology, 84(11):5550-64.

10.  Danthi P1, Coffey CM, Parker JS, Abel TW, Dermody TS. (2008). Independent regulation of reovirus membrane penetration and apoptosis by the mu1 phi domain. PLOS Pathogens, 4(12):e1000248. PLOS Pathogens, 4(12):e1000248.

11.  Ossiboff RJ1, Parker JS. (2007). Identification of regions and residues in feline junctional adhesion molecule required for feline calicivirus binding and infection. Journal of Virology, 81(24):13608-21.

12.  Coffey CM1, Sheh A, Kim IS, Chandran K, Nibert ML, Parker JS. (2006). Reovirus outer capsid protein micro1 induces apoptosis and associates with lipid droplets, endoplasmic reticulum, and mitochondria. Journal of Virology, 80(17):8422-38.

13.  Miller CL1, Parker JS, Dinoso JB, Piggott CD, Perron MJ, Nibert ML. (2004). Source Increased ubiquitination and other covariant phenotypes attributed to a strain- and temperature-dependent defect of reovirus core protein mu2. Journal of Virology, 78(19):10291-302.