Research reveals new insights into how Crimean-Congo hemorrhagic fever virus makes us sick
- 2 min. read ▪ Published
A new paper from researchers at UC Berkeley School of Public Health, Albert Einstein School of Medicine, the US Army Medical Research Institute of Infectious Diseases (USAMRIID), and other institutions, has yielded new insights into how antibodies targeting a specific protein produced by cells infected with Crimean-Congo hemorrhagic fever virus (CCHFV) may be a good candidate for use in future therapies and vaccines for the virus.
CCHFV is a highly lethal tick-borne disease and kills up to 40% of people it infects.
Infections occur through tick bites or by handling the carcasses of infected sheep, goats, and cattle. No vaccines or drugs are available for preventing or treating the disease, which causes increasingly frequent and widespread hemorrhagic-fever outbreaks in Africa, Europe, and Asia.
Cells infected with CCHFV release the viral glycoprotein GP38, which has been considered a promising target for protective vaccines or other treatments because antibodies binding this protein protect against severe cases of CCHFV in animal models. But a lack of knowledge about GP38—what it does and why blocking it may protect people from CCHFV—has hampered efforts to develop medications or vaccines to treat or prevent the virus.
Now, research led by Dr. Eva Harris of UC Berkeley School of Public Health, Dr. Kartik Chandran of Albert Einstein School of Medicine, and Dr. Andrew Herbert of USAMRIID yielded mechanistic insights into why GP38 may be a good target for potential treatments or vaccines.
Using a mouse model, the scientists found that CCHFV infection—as well as GP38 alone—causes fluids to leak from blood vessels, allowing the virus to spread to organs such as the liver and spleen where it can multiply.
Using a panel of monoclonal antibodies targeting different regions of the GP38 protein, the researchers identified the most effective antibodies in protecting mice against blood loss and lethal CCHFV infection.
The findings emphasize the importance of including GP38 antibodies in potential CCHFV vaccines or therapy.
Felix Pahmeier, first author of a paper outlining these research results, said, “This project, which has been a great collaborative effort between academic, government and industry labs, exemplifies the aims of the PROVIDENT consortium, furthering the understanding of how dangerous viruses cause disease and how to best design effective interventions.”
The results were published online on February 19 in Science Translational Medicine—the first publication from the PROVIDENT consortium, a multi-institute, National Institutes of Health-supported collaboration aimed at developing vaccines and treatments against CCHFV and other viral threats.