Welcome to the IUMS 2022 Interactive Program

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The ongoing COVID-19 pandemic has increased awareness about sex-specific differences in immunity and outcomes following respiratory virus infections. Strong evidence of a male bias in COVID-19 disease severity will be presented based on clinical data and preclinical animals models, which illustrate sex differential immune responses against SARS-CoV-2. Prior to the pandemic, data from other viral infections, including influenza viruses, showed profound sex differences in virus-specific immunity, including locally in the respiratory tract. We have used influenza A viruses to interrogate sex-specific immunity to infection and vaccination. Although males are more susceptible to most viral infections, females possess immunological features that contribute to greater vulnerability to immune-mediated pathology but also better protection following vaccination. Both sex chromosome complement and related X-linked genes (e.g., TLR7) as well as sex steroids, including estrogens and androgens, play important roles in mediating the development of sex differences in immunity to respiratory viral infections and vaccination.

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Virus host shifts and the determinants of host range

Emerging infectious diseases are often the result of a host shift, where the pathogen originates from a different host species. Using a panel of up to 50 species of Drosophila we have found the host phylogeny is important for understanding the ability of a virus to infect and cause virulence in a novel host. We have examined how environmental factors such as temperature affect susceptibility, and how the tissue tropism of the virus varies across host species. We have gone on to examine correlations in susceptibility to different related viruses finding evidence for virus-by-host species interactions. Finally we have examined how viruses evolve in related host species.

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Human pandemics, including the ongoing pandemic of SARS-CoV-2 have brought a global focus on wildlife as a reservoirs for a variety of zoonotic diseases. Using wild birds as a as a key example, I will interrogate the virus dynamics in not only the context of “one-host, one-virus” systems, but also extend this towards understanding virus dynamics in “multi-host, multi-virus” systems. The ecology of avian influenza viruses in Mallards, the main reservoir, provide an excellent example of a “one-host, one-virus” system that has been intensively assessed. Indeed, this system has played a key role in disentangling the virus dynamics in Europe and North America. However, avian influenza is a multi-host virus; using wild birds in Australia as a model, I will reveal factors that may dictate host range, and how this may be integrated into our understanding of avian influenza virus ecology. While we have made great strides in understanding the dynamics of socioeconomically important avian viruses like avian influenza, we actually have little appreciation for the diversity of viruses found in wild birds, nor the factors that may modulate the virus communities in wild birds. Indeed, meta-transcriptomic studies have revealed both heterogeneity and connectivity of bird viromes in closely related avian species, and further illustrated that many of the factors important for viruses such as avian influenza may modulate entire virus communities. Overall, birds share our cities, and food production birds are globally with billions of birds raised each year for human consumption. As such, understanding the diversity, ecology and evolution of avian viruses in their wild bird reservoir is imperative.