(160220) -- CARACAS, Feb. 20, 2016 (Xinhua) -- A sanitary employee fumigates against Aedes aegypti mosquito, the vector of zika virus, in Antimano sector of Caracas, capital of Venezuela, on Feb. 19, 2016. A Municipal Day against Zika Virus is held here on Friday. A total of 4,500 suspected cases of the zika virus have been detected in Venezuela by the end of January. (Xinhua/Cristian Hernandez) (djj)
New York, June 22 (IANS) With the help of genetic screens using the groundbreaking genome editing technology CRISPR/Cas9, scientists have discovered human proteins that Zika virus needs for replication and survival.
These findings represent potential therapeutic targets that could help to treat and prevent Zika, dengue and other emerging viral infections.
"These genetic screens give us our first look at what these viruses need to survive," said lead researcher Abraham Brass, Assistant Professor at University of Massachusetts Medical School UMMS) in the US.
"In our lab, we adapted the technology and tools we'd established over the last four years working with other viruses to begin investigating the biology of Zika virus," Brass noted.
Zika, first isolated from an infected macaque in Africa, suddenly emerged in Micronesia in 2007 and expanded its range to Southeast Asia. In May 2015, Zika was identified in Brazil.
With its rapid spread throughout Central and South America, Zika has emerged as a severe health threat that can hamper brain development in newborns, as well as muscle weaknesses in children and adults.
Declared a public health emergency by the World Health Organization, there is no treatment for Zika.
With just a few proteins of their own, Zika and dengue viruses must commandeer a host cell's resources and proteins in order to grow and replicate.
Some antiviral therapies used for HIV and hepatitis C virus work by disrupting the virus' ability to use these resources.
The first step in applying this anti-viral approach to Zika and dengue is to narrow down which of the more than 20,000 human proteins the virus needs to replicate.
The new study published online in the journal Cell Reports is a big step in that direction.
"These viral dependencies on human proteins represent weaknesses that could potentially be used to prevent or stop infection," Brass said.
"Just like any enemy, the more we know about how these viruses function and replicate the better," Brass noted.
