Assistant Professor
Areas of Interest: Virus host interactions; Influenza virus polymerase function
Jonelle Mattiacio
Education:

Ph.D., University of Buffalo Medical School
B.S., SUNY College of Environmental Science and Forestry

Dr. Mattiacio is involved in teaching a variety of courses to freshman, sophomore, junior, and senior students beginning with General Biology lecture during freshman fall semester and culminating in optional elective coursework for seniors. When not in the classroom, you can find her in the lab teaching students how to study and manipulate viruses. Her research interests lie in understanding virus-host interactions using influenza as a model RNA virus.

Teaching

  • BIOL 120 - P4 General Biology
  • BIOL 107L - Microbes and Disease
  • BIOL 214 - Microbiology
  • BIOL 311L - Cell Techniques
  • BIOL 412 - Virology

Research

Viruses are complex pathogens that are responsible for many devastating human diseases. Each year in the US, influenza or “flu” kills more than 36,000 people and hospitalizes 200,000 more. Along with the annual seasonal epidemics, influenza is also responsible for occasional lethal global pandemics, such as those of 1918, 1957, 1968, and the most recent 2009 (swine-origin H1N1). Even though we currently have an effective seasonal influenza vaccine, continued research on influenza biology is essential to find better ways to prevent, diagnose, and treat both seasonal and pandemic influenza.

Viruses are obligate intracellular parasites and therefore depend exclusively on host cellular machinery to replicate. Host cells in turn develop multi-layered antiviral mechanisms to control or prevent viral infection. Studying virus-host interactions is therefore essential for developing more effective virus control strategies. The focus of Dr. Mattiacio’s research is to study influenza-host interactions particularly involving the viral polymerase complex. The viral polymerase complex (3P) consisting of three proteins (PB1, PB2, PA), is responsible for viral mRNA transcription & replication of the viral genome. It is also known to play an important role in viral pathogenesis & host adaptation. The 3P complex assembles in the host cell nucleus, where transcription and replication occur. Several events must occur inside the host cell in order to support viral replication and these events require the viral RNA polymerase to interact with numerous host cell factors, many of which have yet to be identified. In the Mattiacio laboratory, students utilize basic molecular biology techniques (such as PCR, DNA preparation and analysis, gene cloning, protein expression and analysis), mammalian cell culture and luciferase reporter gene assays to investigate these interactions.

Current projects ongoing in the Mattiacio lab:

1. Influenza Polymerase Host Factor Project. From previously published data, the lab has a list of over 100 proteins that were shown to be potential influenza polymerase host cell binding partners. Current work involves examining how a subset of these proteins influences viral replication and pathogenesis, as well as the activity of the viral RNA polymerase complex.

2. Antiviral SLFN11 Restriction of Influenza Viral Protein Production. Host cells develop numerous mechanisms to control or prevent viral infection. Slfn11 is a recently discovered interferon induced antiviral protein that restricts HIV replication by blocking viral protein production. We are investigating the effects of Slfn11 on influenza virus replication and protein production. Some of this work is done in collaboration with Dr. Stephen Dewhurst at the University of Rochester Medical Center.

Publications

  • Sullivan MA, Brooks LR, Weidenborner P, Domm W, Mattiacio J, Xu Q, Tiberio M, Wentworth T, Kobie J, Bryk P, Zheng B, Murphy M, Sanz I, Dewhurst S. 2013. Anti-idiotypic monobodies derived from a fibronectin scaffold. Biochemistry. 52(10): 1802-13.
  • Kobie JJ, Alcena DC, Zheng B, Bryk P, Mattiacio JL, Brewer M, Labranche C, Young FM, Dewhurst S, Montefiori DC, Rosenberg AF, Feng C, Jin X, Keefer MC, Sanz I. 2012. 9G4 autoreactivity is increased in HIV-infected patients and correlates with HIV broadly neutralizing serum activity. PLoS One. 7(4):e35356.
  • Bradel-Tretheway BG*, Mattiacio JL*, Krasnoselsky A, Stevenson C, Purdy D, Dewhurst S, Katze MG. 2011. Comprehensive proteomic analysis of influenza virus polymerase complex reveals a novel association with mitochondrial protein and RNA polymerase accessory factors. J Virol. 85(17): 8569-81.
  • Bussey KA, Desmet EA, Mattiacio JL, Hamilton A, Bradel-Tretheway B, Bussey HE, Kim B, Dewhurst S, Takimoto T. 2011. PA residues in the 2009 H1N1 pandemic influenza virus enhance avian influenza virus polymerase activity in mammalian cells. J Virol. 2011 85(14): 7020-8.
  • Mattiacio J, Walter S, Brewer M, Domm W, Friedman AE, Dewhurst S. 2011. Dense display of HIV-1 envelope spikes on the lambda phage scaffold does not result in the generation of improved antibody responses to HIV-1 Env. Vaccine. 2011 29(14): 2637-47.
  • Mattiacio JL, Read LK. 2009. Evidence for a degradosome-like complex in the mitochondria of Trypanosoma brucei. FEBS Lett. 2009 583(14): 2333-8.
  • Mattiacio JL, Read LK. 2008. Roles for TbDSS-1 in RNA surveillance and decay of maturation by-products from the 12S rRNA locus. Nucleic Acids Res. 36(1): 319-29.
  • Penschow JL, Sleve DA, Ryan CM, Read LK. 2004. TbDSS-1, an essential Trypanosoma brucei exoribonuclease homolog that has pleiotropic effects on mitochondrial RNA metabolism. Eukaryot Cell. 3(5):1206-16.