Faculty member receives NIH grant to study RNA viruses of wildlife
Dr. Andrew Allison, an assistant professor of veterinary virology at the UF College of Veterinary Medicine, has received a two-year, $430,601 exploratory/developmental research grant from the National Institutes of Health’s Institute of Allergy and Infectious Diseases to study RNA viruses of wildlife.
Funding from the grant, known as an R21, will enable Allison to pursue how these viruses capture host genes in order to subvert immune responses and cause disease. The R21 program provides support for the early and conceptual stages of project development.
Starting in 2010, Allison, along with a multi-institutional team from the University of Georgia, University of Pennsylvania, U.S. Fish and Wildlife Service, U.S. Department of Agriculture, and Biodiversity Research Institute began investigating large-scale mortality events in the northeastern United States involving a species of sea duck called the common eider.
“During these outbreaks, which repeatedly occur along the shores of Cape Cod, Massachusetts, most of the birds affected are found dead,” Allison said. “However, sick birds in varying stages of disease are often observed, and these birds exhibit a variety of clinical signs, such as the reluctance or inability to move when approached, labored breathing, and neurological symptoms, including convulsions.”
A new virus designated as Wellfleet Bay virus, which is within the same virus family as influenza viruses, was found to be the primary pathogen causing these outbreaks of disease. However, another novel RNA virus, called Jeremy Point virus, was also found to be co-circulating with Wellfleet Bay virus during these die-offs and is the subject of Allison’s NIH-funded research.
A unique feature of Jeremy Point virus is that in addition to its normal viral genes, it has an extra gene in its genome not found in other related viruses, Allison said, adding that this gene is not viral in origin, as it was acquired, or rather captured, from a vertebrate host.
“You can think of it as a virus stealing a gene from the animal or human it’s infecting and then using that stolen gene to its own advantage in order to continue to spread within that host,” Allison said. “Moreover, the captured gene appears to have also been duplicated by the virus and the duplicated gene is now evolving into a new protein, such that the virus now has two new genes in its arsenal.”
Deciphering the biological role of these two new genes and how the virus uses them against the host it is infecting are the main objectives of Allison’s research.
“Understanding the role that wildlife play in maintaining RNA viruses in nature and how those viruses spread between different wildlife species, domestic animals, and humans has become increasingly important within recent years,” Allison said.
For example, epidemics or pandemics of disease caused by RNA viruses found in wildlife — such as influenza A virus from ducks and shorebirds, Ebola virus from fruit bats, and SARS-related coronaviruses from insectivorous bats — has demonstrated that the cross-species transmission of wildlife viruses to other hosts can have far-reaching global health implications, he said.
“At the same time, it is important to note that wildlife populations play imperative roles in maintaining the balance of ecosystems and thus should be protected, while concomitantly implementing measures to minimize the risk of viral spillover to humans and other animals,” Allison said.
In addition to Allison’s lab, the NIH project also includes the laboratories of Dr. Robert McKenna, a structural biologist in the College of Medicine at UF who uses techniques such as X-ray crystallography to determine the three-dimensional structure of proteins, as well as Dr. Caroline Jones, an expert in immune cell microfluidics at the Erik Jonsson School of Engineering and Computer Science, University of Texas-Dallas. As such, the assembled team provides a multi-disciplinary synergistic approach to investigate the structural-functional aspects of how RNA viruses can evolve to evade the immune responses of the hosts they infect.