Rift Valley Fever Virus (RVFV) is an emerging infection in sub-Saharan and North Africa that causes severe, hemorrhagic illness in livestock and humans and which has pandemic potential.
James Crowe Jr., MD, and colleagues isolated a panel of human monoclonal antibodies from the blood of people in Kenya who had survived RVFV infection and from those who had received an investigational vaccine against the virus.
Monoclonal antibodies recognizing antigenic sites on two glycoproteins on the viral surface had potent neutralizing ability and reduced illness and death in a mouse model of the infection, the researchers reported this week in the Proceedings of the National Academy of Sciences.
These findings suggest a novel mechanism for neutralization — that by preventing the glycoproteins from fusing, or structurally rearranging, the monoclonal antibodies inhibited the ability of the virus to bind to, enter and replicate inside its target cell.
“This work lays the foundation for future therapeutic antibody development,” they concluded.
Funding was provided through contracts with the National Institutes of Health (NIH) and US Department of Health and Human Services, and a Fogarty International Center/NIH grant, TW008067.
