Dengue fever is a mosquito-borne viral disease. A research team has identified how small changes in dengue's viral genome can affect the virus' ability to manipulate human immune defenses and spread more efficiently. The study by Singapore's Duke-NUS Graduate Medical School is the first of its kind that examined the dengue virus starting from broad population level observations and then linked it to specific molecular interactions, to explain a dengue outbreak.
This research work provides a framework for identifying genomic differences within the virus that are important for epidemic spread. Scientists identified how a new strain of dengue serotype 2 virus (DENV-2) emerged and completely displaced an older strain of DENV-2 during the 1994 dengue epidemic in Puerto Rico.
The research team found three mutations in the tail of the dengue genome that enabled the virus to make short fragments of genomic material, which consisted exclusively of its tail. The tail is how the dengue virus got its sting or potency, as it was the tail that bound to a protein and suppressed the human antiviral response. The suppressed human antiviral response allowed the new strain of DENV-2 to then spread more efficiently within an infected individual and increased its chances of infecting fresh mosquitoes for the virus transmission.
The study suggests that combining population studies with molecular investigations result in genetic information that explains virus evolution better, and that could be further developed into a predictor of epidemics. Lead researcher Eng Eong Ooi added, "The findings imply that identifying the molecular signatures that allow the viruses to spread more efficiently could help focus public health resources on more important strains of viruses."
The study appears in Science.