Scientists now know how Zika and dengue viruses assemble inside host, will improve vaccine and antiviral efforts

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GALVESTON, Texas – Two new studies from The University of Texas Medical Branch at Galveston have unraveled the mystery of how the dengue and Zika viruses assemble when they infect human and mosquito hosts. The results have recently been published in Cell Host & Microbe (for dengue virus) and mBio (for Zika virus).

“These findings represent major progress toward understanding how these deadly viruses are assembled during infection, which provides new opportunities for antiviral and vaccine development,” said Pei-Yong Shi, UTMB professor in the department of biochemistry & molecular biology.

In summary, now that scientists know how Zika and dengue viruses form inside infected cells, this knowledge could be used to deter or stop the viruses from gaining full strength through inhibiting virus formation.

Like dengue and Zika viruses, many closely related flaviviruses cause frequent epidemics around the world, including West Nile, yellow fever, and tick-borne encephalitis viruses. These viruses share a common structure containing 180 copies of structural proteins on the virus surface and an interior viral genome. No one knew how the viral structural proteins and genome are assembled into virus particles within infected cells.

“Using biochemical, microscopic imaging and virological methods, we demonstrated that a viral protein called NS2A orchestrates the virus assembly by recruiting the structural proteins, viral genome and viral enzyme called protease to the assembly site,” says Xuping Xie, a UTMB research scientist who co-directed the two studies. “At the assembly site, the viral protease cuts down a structural protein pre-cursor into mature proteins that bind to the viral genome to form a new virus. So, the assembly of these viruses are closely regulated by the viral protease.”

“Virus assembly is an understudied research topic. It is remarkable to see that the results from dengue and Zika viruses share a common assembly mechanism,” says Mariano Garcia-Blanco, Professor at UTMB who is not directly involved in the studies. “Once the assembly mechanism has been defined, one could design inhibitors to block virus assembly for antiviral development and to rationally engineer virus for vaccine development.”


The University of Texas Medical Branch at Galveston


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