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The Impact of Prior Flavivirus Infections on the Development of Type 2 Diabetes Among the Indigenous Australians

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  • 1 College of Public Health, Medical and Veterinary Sciences, James Cook University, Queensland, Australia.
  • | 2 College of Healthcare Sciences, James Cook University, Queensland, Australia.
  • | 3 Anton Breinl Research Centre for Health Systems Strengthening, James Cook University, Queensland, Australia.
  • | 4 School of Chemistry and Molecular Biosciences, University of Queensland, Queensland, Australia.

It is estimated that 5% of Australians over the age of 18 have diabetes, with the number of new cases increasing every year. Type 2 diabetes (T2D) also represents a significant disease burden in the Australian indigenous population, where prevalence is three times greater than that of non-indigenous Australians. Prevalence of T2D has been found to be higher in rural and remote indigenous Australian populations compared with urban indigenous Australian populations. Several studies have also found that body mass index and waist circumference are not appropriate for the prediction of T2D risk in indigenous Australians. Regional and remote areas of Australia are endemic for a variety of mosquito-borne flaviviruses. Studies that have investigated seroprevalence of flaviviruses in remote aboriginal communities have found high proportions of seroconversion. The family Flaviviridae comprises several genera of viruses with non-segmented single-stranded positive sense RNA genomes, and includes the flaviviruses and hepaciviruses. Hepatitis C virus (HCV) has been shown to be associated with insulin resistance and subsequent development of T2D. Flaviviruses and HCV possess conserved proteins and subgenomic RNA structures that may play similar roles in the development of insulin resistance. Although dietary and lifestyle factors are associated with increased risk of developing T2D, the impact of infectious diseases such as arboviruses has not been assessed. Flaviviruses circulating in indigenous Australian communities may play a significant role in inducing glucose intolerance and exacerbating T2D.

Author Notes

* Address correspondence to Alanna Sorenson, College of Public Health, Medical and Veterinary Sciences, Building 94, Solander Drive, James Cook University, Townsville, Queensland 4811, Australia. E-mail: alanna.sorenson@jcu.edu.au

Authors' addresses: Alanna Sorenson and Leigh Owens, College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, Queensland, Australia, E-mails: alanna.sorenson@jcu.edu.au and leigh.owens@jcu.edu.au. Marie Caltabiano, College of Healthcare Sciences, James Cook University, Cairns, Queensland, Australia, E-mail: marie.caltabiano@jcu.edu.au. Yvonne Cadet-James, Anton Breinl Research Centre for Health Systems Strengthening, James Cook University, Townsville, Queensland, Australia, E-mail: yvonne.cadetjames@jcu.edu.au. Roy Hall, School of Chemistry and Molecular Biosciences, University of Queensland, Queensland, Australia, E-mail: roy.hall@uq.edu.au. Brenda Govan and Paula Clancy, College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, Queensland, Australia, E-mails: brenda.govan@jcu.edu.au and paula.clancy@jcu.edu.au.

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