Viral Immunity and Immunopathology

Viral Immunity and Immunopathology Research Group

Research Group Head

The Viral Immunity and Immunopathology group focuses on understanding the mechanisms involved in the induction and regulation of innate immune responses during viral infections.

One focus is influenza A virus (IAV), the virus responsible for the ‘flu’. There is a continual threat that novel influenza A viruses IAV will be transmitted from birds to humans, an occurrence called ‘cross-over’. These severe infections involving highly pathogenic IAV are associated with hyperinflammatory responses, immunopathology and high mortality rates (30-40 per cent).

Innate immune responses play an important role in providing protection during viral infections, such as those involving IAV. However, an overreaction of the innate immune system, such as that seen during severe IAV infection, causes cellular and tissue damage. Patients often present to hospital with severe disease, several days after the onset of symptoms. There are currently no effective or targeted drugs or therapies in use to limit immunopathology and disease at this stage of the infection.

Utilising a range of preclinical models and techniques, Dr Tate and her team aim to gain a greater understanding of the mechanisms involved in inducing and regulating a hyperinflammatory response in order to identify novel therapeutic targets.

Research Group

Selected publications

  • Tate MD, Ong JD, Dowling JK, McAuley JL, Robertson AB, Latz E, Drummond GR, Cooper MA, Hertzog PJ, Mansell A (2016) Reassessing the role of the NLRP3 inflammasome during pathogenic influenza A virus infection via temporal inhibition. Sci Rep 6:27912.

  • Tate MD, Job ER, Deng YM, Gunalan V, Maurer-Stroh S, Reading PC (2014) Playing hide and seek: how glycosylation of the influenza virus hemagglutinin can modulate the immune response to infection. Viruses 6:1294-1316.

  • Thomas BJ, Porritt RA, Hertzog PJ, Bardin PG, Tate MD (2014) Glucocorticosteroids enhance replication of respiratory viruses: effect of adjuvant interferon. Sci Rep 4:7176.

  • McAuley JL, Tate MD, MacKenzie-Kludas CJ, Pinar A, Zeng W, Stutz A, Latz E, Brown LE, Mansell A (2013) Activation of the NLRP3 inflammasome by IAV virulence protein PB1-F2 contributes to severe pathophysiology and disease. PLoS Pathog 9:e1003392.

  • Tate MD, Brooks AG, Reading PC, Mintern JD (2012) Neutrophils sustain effective CD8+ T-cell responses in the respiratory tract following influenza infection. Immunol Cell Biol 90:197-205.

  • Tate MD, Brooks AG, Reading PC (2011) 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 187:1884-1894.

  • Tate MD, Ioannidis LJ, Croker B, Brown LE, Brooks AG, Reading PC (2011) The role of neutrophils during mild and severe influenza virus infections of mice. PLoS One 6:e17618.

  • Tate MD, Job ER, Brooks AG, Reading PC (2011) Glycosylation of the hemagglutinin modulates the sensitivity of H3N2 influenza viruses to innate proteins in airway secretions and virulence in mice. Virology 413:84-92.

  • Tate MD, Pickett DL, van Rooijen N, Brooks AG, Reading PC (2010) Critical role of airway macrophages in modulating disease severity during influenza virus infection of mice. J Virol 84:7569-7580.

  • Tate MD, Deng YM, Jones JE, Anderson GP, Brooks AG, Reading PC (2009) Neutrophils ameliorate lung injury and the development of severe disease during influenza infection. J Immunol 183:7441-7450.