A single mutation may explain why Zika suddenly erupted from obscurity to become the alarming re-emerging infectious disease it is today.
According to researchers from Texas and China, the mutation boosts Zika’s ability to hop into feasting mosquitoes that can then shuttle the virus to more victims. Based on archived viral strains, the mutation popped up sometime between the virus’ low-profile outbreaks in Southeastern Asia (which took place in 2007 and 2012) and Zika’s explosive emergence in the Americas beginning in 2015.
In experiments with mosquito-bitten, Zika-infected mice, the researchers quickly noticed that the 2016 virus was far better at infecting Aedes aegypti mosquitoes (a main Zika carrier) than the 2010 virus. The 2016 virus also produced much higher levels of a protein called “nonstructural protein 1,” or NS1.
The researchers traced the boosted NS1 levels to a specific mutation in the gene that codes for the protein. The mutation…was present in the explosive 2016 Zika virus but absent from its tamer 2010 relative. In cell experiments, the researchers found that this substitution mutation alone could switch NS1 levels from low to high. But they don’t know why, exactly.
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