Like many other viruses, Rift Valley fever virus causes disease in animals and can be transmitted to humans by infected mosquitos or through contact with the blood or organs of infected animals. Scientists at Utah State University’s Institute for Antiviral Research, in collaboration with researchers at Vanderbilt University Medical Center, conducted studies that identified specific monoclonal antibodies from people who were previously infected with or immunized against RVFV that successfully neutralized the virus in animal models. The work was recently published in the Proceedings of the National Academy of Sciences.
While outbreaks of Rift Valley fever virus (RVFV) typically occur in sub-Saharan and North Africa, cases have also been confirmed in the Arabian Peninsula. And as people have seen and experienced with other virus-caused diseases, viruses don’t stop at a country’s border and are only a few carriers away from spreading far beyond their original location.
Outbreaks of RVFV, which is most commonly seen in domesticated animals, result in livestock deaths and abortions in pregnant females, causing large economic losses. According to the World Health Organization, when the virus infects humans it causes illness ranging from mild influenza-like symptoms to potentially lethal hemorrhagic fever which is characterized by bleeding and the failure of many organs and systems in the body.
USU Institute for Antiviral Research (IAR) Senior Researcher Jonna Westover and IAR Director, Professor Brian Gowen contributed to the project employing a RVFV mouse infection model evaluating the ability of anti-RVFV monoclonal antibodies to prevent infection. They specifically looked at antibodies directed at the protein on the surface of the virus that mediates its ability to attach to a host cell, the first step in the infection process. The paper notes the antibodies did bind to specific regions of the surface of the virus, blocking its ability to cause infection.
“While this is the first time we have evaluated monoclonal antibodies as a candidate antiviral intervention for RVFV infection, we continue to work on several monoclonal antibody therapeutics projects aimed at blocking Junin virus infection, which can lead to an often lethal viral hemorrhagic fever syndrome,” Gowen said.
According to the U.S. Centers for Disease Control and Prevention, RVFV is difficult to control because animals develop high viral loads in their blood which makes it easy for mosquitoes to become infected and spread the virus to other animals and humans. The virus is also considered a viable bioterrorist weapon.
Westover and Gowen explained that the binding of the monoclonal antibodies targeted three different sites on the surface of RVFV particles, an important proof-of-concept that supports efforts to continue to develop therapeutic antibodies to prevent and treat RVFV infections.
“Combining multiple antibodies would greatly limit escape mutants of the virus that can arise because of selective pressure from treatment with a single antibody,” Gowen said. “Such mutants could effectively evade neutralization and not respond to treatment.”
The world’s attention has been on the SARS CoV-2 coronavirus for more than a year. Gowen said virus outbreaks of any kind underscore the need to be better prepared for other emerging viral diseases that can make their way into new populations of animals and people who have no immunity.
“I think what most experts can agree on is that humanity will face many more threats and challenges posed by viruses,” Gowen said. “It’s no longer a question of “if”, it’s a matter of “when.”
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Institute for Antiviral Research
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