Viral Immunopathology Unit
Lab head: Professor Nicholas King
Location: Blackburn Building, Camperdown
Research conducted by this unit focuses on the immunobiology of cell membrane surfaces, with particular emphasis being placed on studying the processes which control cell membrane architecture and the modulation of cell surface molecules (specifically, those which are involved in immune cell interactions). Much of the work carried out in this laboratory concerns the flavivirus, West Nile Virus, which curiously brings about an increase in major histocompatibility, as well as increased antigen and adhesion molecule expression in mammalian cells following infection. For a virus, this is a seemingly suicidal action, because this increases the efficiency of the adaptive immune response. However it is clear that the adaptive immune response contributes to the pathogenesis of disease; that is, the anti-viral immune response causes immunopathology.
The role of mucosal dendritic cells in controlling virus infection in epithelium
Primary supervisor: Nicholas King
In a sexually transmitted disease (STD) model of virus infection in the mouse we find that infection by this route results in excellent immunity and very low mortality, compared to other routes on infection. Why is this so successful at this site? Understanding this is crucial for the development of effective vaccines.
We have found that the dendritic cells (DC) in the vaginal tissue accumulate where the virus infection is greatest in the epithelium and these DC disperse once the infection is eradicated. However, DC gather more quickly upon a second challenge with the same virus. What factors make them accumulate in this accelerated manner? Do these DC have antiviral activities? We are measuring how and when these cells immigrate into the vaginal epithelium and how they migrate from here to the local draining lymph nodes after infection to enable the antiviral immune response to be initiated. We are asking how this is different on the second challenge with the same virus. Using this model we are investigating if these steps involved in generating long-lasting antiviral immune memory responses at this site are the reasons for better survival.