In a new study, researchers identified a subgroup of antibodies responsible for dengue’s increased deadliness upon second exposure.
People with pre-existing antibodies against dengue are more likely to experience severe symptoms.
The cases of dengue fever are on rise globally with an increase in number of people battling severe symptoms. This has necessitated the development of a universal dengue vaccine that can safeguard people from this deadly infection. The peculiar thing about dengue is that it is deadlier in case of repeat infection and the chances of developing a life-threatening disease is higher the second time.
Our bodies not only fail to get protection due to earlier infection but also become more susceptible to a deadlier infection; why this happens has been a mystery that scientists have been trying to uncover. In a new research published in Nature Microbiology, researchers identified a particular subgroup of antibodies responsible for dengue’s increased deadliness upon second exposure. This could open the door for development of a universal dengue vaccine that can benefit millions.
People with pre-existing antibodies against dengue are more likely to experience severe symptoms. These antibodies were thought to enhance the virus’s infection of certain immune cells. Recent studies found that these antibodies are linked to the severity of the disease. To understand how these antibodies cause dengue-related issues, scientists created a mouse model that mimics human immune reactions. In these mice, they discovered that harmful effects of dengue antibodies were linked to specific immune cells in the spleen. This highlights the role of these antibodies in dengue and has important implications for developing safer vaccines and treatments.
“We definitively proved that it’s not the presence of dengue antibodies that are a problem, but the quality of those antibodies,” said Stylianos Bournazos, a research associate professor in the laboratory of Jeffrey Ravetch, the Theresa and Eugene M. Lang Professor at Rockefeller.
“Now that we know the pathway that these antibodies use, we can develop therapeutics against it,” the research associate added.
Researchers found that they have to trace the entire pathway of infection and not just focus on the antibodies. The team discovered that severe outcomes of dengue virus weren’t a product of its ability to infect more cells but from the activation of a pathway leading to increased inflammation.
“The findings upended the existing model of dengue infection, demonstrating that a small cadre of essentially “pathogenic” antibodies were primarily responsible for severe infection. The team’s findings indicate that it might be possible to prevent severe disease complications by administering a drug that can deactivate these harmful antibodies,” said a Rockefeller University article.
