| 
			 
						
						
						 A 
						single genetic glitch may explain how Zika became so 
						dangerous 
			
   
            
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		[September 29, 2017] By 
		Julie Steenhuysen 
			
		CHICAGO (Reuters) - A single genetic change 
		that occurred in 2013 may explain how Zika acquired the ability to 
		attack fetal nerve cells, causing a severe birth defect in babies whose 
		mothers were infected while pregnant, Chinese and U.S. researchers 
		reported on Thursday. 
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			 Scientists have posited many theories about why Zika, a 
			mosquito-borne virus that had been linked with only mild symptoms 
			since its discovery in 1947, could suddenly be associated with 
			thousands of cases of the birth defect known as microcephaly, as it 
			was in Brazil in 2015. 
			 
			That outbreak prompted the World Health Organization to declare Zika 
			a public health emergency in 2016, and set off a scientific quest to 
			determine whether Zika could cause microcephaly, a condition marked 
			by small head size. 
			 
			Several teams have already traced the virus circulating in Brazil 
			and elsewhere in South America to a strain of Zika that had been 
			quietly circulating in Southeast Asia for decades. 
			  
			In the new study, published in Science, Ling Yuan of the Chinese 
			Academy of Sciences and colleagues compared genetic changes in 
			samples of the South American virus with one isolated in 2010 in 
			Cambodia. 
			 
			They created seven sample viruses, each with a single genetic 
			difference from the Cambodian strain, and tested these in brains of 
			fetal mice. Although the viruses caused some degree of damage in 
			all, those infected with a virus that carried a single mutation in a 
			structural protein called prM developed severe microcephaly. That 
			strain also proved more lethal to fetal brain cells. 
			 
			The team estimates the genetic change occurred in May 2013, just 
			before a French Polynesian outbreak of Zika in which the first cases 
			of microcephaly and Guillain-Barre, a rare neurological disorder, 
			were noted. 
			
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			"Our findings offer an explanation for the unexpected causal link of 
			Zika to microcephaly, and will help understand how Zika evolved from 
			an innocuous mosquito-borne virus to a congenital pathogen with 
			global impact," Yuan and colleagues wrote. 
			 
			One study author, Dr. Pei-Yong Shi of the University of Texas 
			Medical Branch in Galveston, Texas, said other mutations also fueled 
			the explosive epidemic, including one he and others reported on in 
			May in the journal Nature that enhanced Zika's ability to infect 
			Aedes aegypti mosquitoes, which carry the virus. 
			 
			Last November, WHO pronounced Zika no longer an international 
			emergency, but stressed that the virus, found in at least 60 
			countries, will keep spreading where mosquitoes that carry Zika are 
			present. 
			 
			(Reporting by Julie Steenhuysen; editing by Susan Thomas) 
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