|Academic Degrees||Contact Details|
|1991: BSc (Hons), Department of Microbiology and Immunology, The University of Melbourne,
1997: PhD, Department of Microbiology and Immunology, The University of Melbourne, Australia
2008 - present: Honorary Research Fellow & Educator (50%:50% joint appointment) at WHO Collaborating Centre for Reference and Research on Influenza, VIDRL, North Melbourne
|Tel: +61 3 8344 3437
Fax: +61 3 8347 1540
Room 3.15, Department of Microbiology and Immunology
Or: WHO Collaborating Centre for Reference and Research on Influenza, Victorian Infectious Diseases Reference Laboratories (VIDRL), 10 Wreckyn St, North Melbourne, 3051
2006 - 2011: NHMRC RD Wright Research Fellow, Department of Microbiology and Immunology, University of Melbourne
2004 - 2006: CR Roper Fellow, Department of Microbiology and Immunology, University of Melbourne
2003 - 2004: NHMRC CJ Martin Fellow, Department of Microbiology and Immunology, University of Melbourne
2001 - 2002: Royal Society Howard Florey Fellow, Imperial College School of Medicine, London, UK
Throughout his research career, Patrick has maintained a keen interest in understanding the role of the innate immune system in early protection against viral infections. His PhD studies examining the sensitivity of different viruses to innate host defences was awarded the Chancellor’s Award for Excellence in the PhD thesis. His post-doctoral training at the Sir William Dunn School of Pathology in Oxford focussed on understanding the mechanisms by which poxviruses evade host responses to infection. He returned to the University of Melbourne in 2003 and since this time his research has examined different aspects of influenza virus pathogenesis and disease.
Since mid-2008, Patrick has held joint (50%:50%) appointments as a Research Fellow at the University of Melbourne and as an Educator at the WHO Collaborating Centre for Reference and Research on Influenza. In the latter role, he has been working with a number of partner organizations to enhance laboratory-based detection of influenza, as well as pandemic planning and preparedness, in the Asia/Pacific Region. These activities complement his research into influenza biology and highlight a broader interest in understanding global and public health implications of this disease.
Our research aims to determine how the body first recognizes and responds to influenza viruses and how virus strains of high virulence have adapted to evade detection and destruction by these early (or innate) immune defenses.
1 Soluble barriers to influenza virus infection
Respiratory secretions contain a number of different proteins of the innate immune system - including members of the collectin, pentraxin and defensin superfamilies - that mediate antiviral activity against influenza virus. Detailed information regarding the mechanisms by which these proteins inactivate virus and their role in antiviral defence in vivo are lacking. Current studies aim to identify natural inhibitors of IAV in the airways of mice, ferrets and humans. As mice and ferrets represent the best-characterized animal models of influenza infection, the proposed studies will provide important information when assessing the relevance of each model to understanding human disease.
2 Cell surface receptors for attachment and entry of influenza virus into cells of the innate immune system
Airway macrophages and dendritic cells (DC) are important components of innate host defense and play a critical role in limiting the severity of influenza infection. Detailed information regarding the mechanisms by which macrophages and DC recognize influenza virus for attachment, uptake and destruction are lacking. Our group has recently identified specific receptors involved in influenza virus infection of macrophages and DC. We now aim to investigate virus-encoded and host-encoded determinants that modulate efficiency of virus binding and infection. These studies will provide novel information regarding how influenza virus is first recognized by cells of the innate immune system as well as insight into why virulent strains circumvent uptake and destruction by macrophages and DC.
3 The role of innate immune cells in protection and pathology during influenza virus infection
Infection of respiratory epithelium and airway macrophages/DC results in the release of a range of chemokines and cytokines, which in turn leads to the recruitment of innate inflammatory cells such as neutrophils and natural killer cells to the airways. We are interested in understanding factors governing the recruitment, activation and role of innate inflammatory cells during influenza infections. While innate immune cells are generally associated with resolution of infection, dysregulated recruitment and activation of innate cells can contribute to pulmonary pathology and disease.
Dr Sarah Londrigan
Emma Job (PhD student)
Wy Ching Ng (PhD student)
Kirsty Short (PhD student)
- Londrigan SL, Tate MD, Brooks AG, Reading PC. Cell-surface receptors on macrophages and dendritic cells for attachment and entry of influenza virus. J Leuk Biol 2011 Nov; Epub ahead of print
- Short KR, Diavatopoulos DA, Thorton DA, Pedersen SJ, Strugnell RA, Wise A, Reading PC, Wijburg OL. Influenza virus induces bacterial and non-bacterial otitis media. J Inf Dis 2011; 204(12): 1857-65.
- Tate MD, Brooks AG, Reading PC. Specific Sites of N-linked Glycosylation on the hemagglutinin of H1N1 subtype influenza A virus determine sensitivity to inhibitors of the innate immune system and virulence in mice. J Immunol 2011; 187(4): 1884-94.
- Tate MD, Brooks AG, Reading PC, Mintern JM. Neutrophils are required for sustained CD8+ T cell responses in the respiratory tract following influenza virus infection. Immunol Cell Biol 2011 April; Epub ahead of print.
- Short KR, Diavatopoulos DA, Reading PC, Brown LE, Rogers KL, Strugnell RA, Wijburg OL. Using Bioluminescent Imaging to Investigate Synergism Between Streptococcus pneumoniae and Influenza A Virus in Infant Mice. J Vis Exp 2011; 50 pii: 2357.
- Tate MD, Job ER, Brooks AG, Reading PC. Glycosylation of the Hemagglutinin Modulates the Sensitivity of H3N2 Influenza Viruses to Innate Proteins in Airway Secretions and Virulence in Mice. Virology 2011; 413(1): 84-92.
- Tate MD, Brooks AG, Reading PC. Receptor Specificity of the Influenza Virus Hemagglutinin Modulates Sensitivity to Soluble Collectins of the Innate Immune System and Virulence in Mice. Virology 2011; 413(1): 128-38.
- Tate MD, Ioannidis LJ, Croker B, Brown LE, Brooks AG, Reading PC. The Role of Neutrophils During Mild and Severe Influenza Virus Infection of Mice. PLoS ONE 2011; 6(3): e17618.
- Tate MD, Schilter HC, Brooks AG, Reading PC. Responses of Mouse Airway Epithelial Cells and Alveolar Macrophages to Virulent and Avirulent Strains of Influenza A Virus. Viral Immunology 2011; 24(2): 77-88.
- Tate MD, Brooks AG, Reading PC. Correlation Between Sialic Acid Expression and Infection of Murine Macrophages by Different Strains of Influenza Virus. Microbes and Infection 2011; 13(2): 202-207.
- Londrigan SL, Turville SG, Tate MD, Deng Y, Brooks AG, Reading PC. DC-SIGN and L-SIGN can Mediate Sialic Acid-Independent Infection of Cells by Influenza A Virus. J Virol 2011; 85(6): 2990-3000.
- Tate MD, Brooks AG, Reading PC. Inhibition of Lectin-Mediated Innate Host Defences In Vivo Modulates Disease Severity During Influenza Virus Infection. Immunol Cell Biol 2011; 89(3): 482-91.
- Job ER, Deng Y, Tate MD, Bottazzi B, Crouch EC, Dean M, Brooks AG, Reading PC. Pandemic H1N1 Influenza A Viruses are Resistant to the Antiviral Activities of Innate Immune Proteins of the Collectin and Pentraxin Superfamilies. J Immunol 2010; 185(7): 4284-91.
- Tate MD, Pickett DL, van Rooijen N, Brooks AG, Reading PC. The Critical Role of Airway Macrophages in Modulating Disease Severity During Influenza Virus Infection of Mice. J Virol 2010; 84: 7569-7580.
- Upham JP, Pickett DL, Irimura T, Anders EM, Reading PC. Macrophage Receptors for Influenza A Virus: Role of the Macrophage Galactose-type Lectin and Mannose Receptor in Viral Entry. J Virol 2010; 84(8): 3730-3737.
- Reading PC, Whitney PG, Pickett DL, Tate MD, Brooks AG. Influenza viruses differ in ability to infect macrophages and to induce a local inflammatory response following intraperitoneal injection of mice. Immunol Cell Biol 2010; 88(6); 641-650.
- Wojtasiak M, Pickett DL, Tate MD, Bedoui S, Job ER, Whitney PG, Brooks AG, Reading PC. Gr-1+cells, but not Neutrophils, Limit Virus Replication and Lesion Development Following Flank Infection of Mice with Herpes Simplex Virus type-1 Infection. Virology 2010; 407(1): 143-51.
- Wojtasiak M, Pickett DL, Tate MD, Londrigan SL, Bedoui S, Brooks AG, Reading PC. Depletion of Gr-1+, but not Ly6G+, Immune Cells Exacerbates Virus Replication and Disease in an Intranasal Model of Herpes Simplex Virus type-1 Infection. J Gen Virol 2010; 91: 2158-2166.