While searching for a new approach to vaccine development for the dengue virus, researchers have discovered that the dengue virus changes its shape by mutations in the envelope protein to escape vaccines and therapeutics.
DENV2 (Dengue Virus) is a soft spherical surface of cells when the mosquito’s body temperature increases (29 ° C). It then converts to bumpy cells at human body temperature (37 ° C).
This ability to morph helps the virus to escape the human host’s immune system. Therefore, a study published in the journal ‘PLOS Pathogens’ reports that it is important to understand the mechanism behind it for therapeutic and vaccine development.
“In laboratory-developed DENV2 strains, with Professor Pei-Yong Shi from the UTMB, we found that the E mutations of the virus transform into bumpy cells. These structural changes make vaccines and therapeutics ineffective against the virus,” says Duke-NUS ) Is the lead author of the study, Xin-ni Lim said.
The team also tested four DENV2 strains obtained from patients. In contrast to laboratory-adapted viruses, they observed that most of these clinical strains maintain a smooth surface structure at 37 ° C. However, at a fever temperature of 40 degrees Celsius, all virus strains hit the bumpy surface.
“Our study provides a new direction for vaccine development and treatment of dengue. Patients should be used with vaccines given before dengue infection, effective against the soft surface virus,” said Dr. Sheemi Lok, professor, Duke-NUS’s EID and author of the study.
“When it comes to patients exhibiting fever symptoms, treatment strategies should be implemented against bumpy epithelial cells,” said Dr. Lok.
“This study is the first step to gain a better understanding of how DENV2 responds and adapts to the host’s immune defenses. We have also been able to use computational modeling methods to assess why different DENV2 species are more or less adept at morphing from cells.
By understanding, Ant We will be able to develop better treatments and vaccines to treat or prevent diseases and contribute to public health outcomes, ”said Dr. Peter Bond, Principal Investigator from AStarBII.
The results of the study showed that the laboratory is not a good model for DENV2 research, as its structure differs from the clinical strains isolated from patients. The team plans to study other DENV serotypes to see if there are any structural changes.