The findings imply that identifying molecular signatures that allow viruses to spread more efficiently help focus public health resources on the important strains.

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.
Source-ANI