Dr. Christopher Basler, a professor in the Institute for Biomedical Sciences at Georgia State University, director of the university’s Center for Microbial Pathogenesis and a Georgia Research Alliance Eminent Scholar in Microbial Pathogenesis, has received a two-year, $419,100 federal grant to study a virus similar to Ebola virus that causes disease in animals but not in humans.
Basler and his co-investigator, Dr. Thomas Geisbert of the University of Texas Medical Branch at Galveston, will use the grant from the National Institute of Allergy and Infectious Diseases of the National Institutes of Health to study Reston ebolavirus (Reston virus).
“This is a virus that resembles Ebola virus, but what makes Reston virus interesting and unique is that whereas Ebola virus, formally Zaire Ebola virus, is typically very deadly in people, Reston virus does not make people sick, but it can still be deadly in some monkeys,” Basler said. “Reston is a virus for which there have been a number of documented human exposures, but people have never gotten sick. The virus is of interest in that respect.”
In the virus family called filoviruses (single-stranded RNA viruses), there are five different species of Ebola virus, which have similar genomic structures but are clearly distinct from each other. Ebola virus and Reston virus are two of the five different species, and Reston virus is the most different from the rest.
Reston virus was originally discovered during an outbreak in monkeys that were brought to an animal facility in Reston, Va. from the Philippines. The monkeys developed a hemorrhagic disease, which investigators found was similar to Ebola virus. The people who were in contact with the animals were monitored closely and showed evidence of being exposed to the virus, but no one became ill. The virus has also been found in pigs.
Reston virus appears to come from a different geographic location than other similar viruses. While outbreaks of Ebola virus and other filoviruses have occurred in Africa, Reston virus seems to originate in the Philippines and China. Presumably, Ebola virus and Reston virus evolved from a common ancestor, but for whatever reason, Reston virus has existed in a different place and seems to be less virulent in people.
“We’re trying to do two things with this project,” Basler said. “One is we’re trying to better understand how the virus grows, the mechanisms by which it replicates and how the disease that it causes in animals differs from what you see with Ebola virus.
“I would argue that if you have different, but similar viruses that cause different types of disease or have different capacities to cause disease, if we can understand what’s different, then maybe that would suggest ways to reduce the severity of the disease.”
In addition, the researchers will apply some of their previous work on Ebola virus to Reston virus. They’re interested in the protein VP35, found in Ebola and other filoviruses, which suppresses immune response and allows the virus to grow, spread and cause disease. They’ve previously identified mutations that can be inserted into VP35 to disable this function in Ebola virus and make the virus unable to cause the disease in animals.
“Innovative approaches are needed to conduct research on frequently deadly filoviruses,” Basler said. “We want to see if we can apply the same approach to Reston virus and make a Reston virus that doesn’t cause disease in animals. The logic behind doing that is Reston virus should already be safer to work with than Ebola virus. If we can build mutations that disable this one function, you have a virus that would still be able to replicate itself but with even less risk of causing disease. Then you’ll have an even safer system that you can use to study how these viruses grow and interact with the host that they infect.”