Poster Presentation Lorne Infection and Immunity 2018

Understanding the mechanisms involved in host permissivity to Ross River and Barmah Forest viruses. (#144)

Penny Rudd 1 , , Helle Bielefeldt-Ohmann 2 , Cheryl A Johansen 3 , David W Smith 4 , Stacey Lynch 5 , Belinda Louise Herring 6 , John Haniotis 7 , Stephen Doggett 7 , Linfa Wang Wang 8 , Lara Herrero 1
  1. Griffith University, Southport, QLD, Australia
  2. School of Veterinary Science, University of Queensland, Gatton, QLD , Australia
  3. PathWest Laboratory Medicine WA, Nedland, , WA, Australia
  4. Faculty of Medicine and Health Sciences , University of Western Australia,, Crawley, Western Australia, Australia
  5. Microbial Sciences, Pests & Diseases,, , Agriculture Victoria Research, Bundoora, Victoria, Australia, Victoria, Australia
  6. Arbovirus surveillance and mosquito monitoring program, Westmead Hospital, Westmead, New South Wales, Australia
  7. Arbovirus surveillance and mosquito monitoring program, Westmead Hospital, Westmead, New South Wales, Australia
  8. Emerging Infectious Diseases Program, , Duke-NUS, Singapore

Each year, Ross River virus (RRV) and Barmah Forest virus (BFV) leave thousands of Australians in chronic debilitating pain. Symptoms include joint/muscle pain, fatigue, fever and rash (1). RRV is known to be maintained primarily in a cycle between mosquitoes and macropods, though less is known about the BFV cycle. However, both have been shown to be capable of infecting other mammals, including other marsupials, rodents, flying foxes, cats, dogs, sheep, cattle and horses (1,2). The contribution of these other hosts to the risk of RRV/BFV infection is yet to be determined, but may be important in the control of the diseases and in predicting the risk of spread into different ecosystems and countries.

Our goal is to understand how RRV, and possibly BFV, can persist in new areas and identify mechanisms involved in establishing reservoir hosts. We investigated the permissiveness of various cell lines to field isolates of RRV and to the prototype of BFV. RRV replicated to high titres in mosquito, cow and bat cells while dog cells only supported low levels of replication. Also we determined the seroprevalence of RRV and BFV in horses (E. caballus) and black flying foxes (P. alecto) around the Brisbane area. We found that 40% of flying foxes were IgG positive for RRV (n=30 total tested) and 7.7% were IgG positive for BFV (n=35) whilst 100% of horses (n=15) were IgG positive for RRV and 40% were IgG positive for BFV (n=5). To elucidate mechanisms that contribute to permissivity to these viruses, we are undertaking a series of glycan and lectin arrays. The lectin/glycan signature mediates key interactions at the virus-host interface, controlling important functions like viral spread and/or activation of the immune system.

We are equally interested in investigating the role of host immune factors such as interferons and interferon stimulated genes on RRV and BFV replication. Certain reports documented an increase only in IFN-b and not IFN-a following infection of Pteropus alecto cells. Our findings may help to better understand the interactions between alphaviruses and the innate immune system of their reservoir hosts. These mechanisms may also be essential to identify key interactions that explain the reservoir competence of certain vertebrate species.