As a cellular protein that interacts with invading viruses appears to help enable the infection process of the Zika virus, according to an international team of researchers who suggest this protein could be a key target in developing new therapies to prevent or treat Zika virus infection.
The study first isolating Zika; a member of the Flaviviridae family of viruses which also includes yellow fever; dengue and West Nile viruses in 1947 and, until recently; it typically caused only mild symptoms in humans. However, health officials first recorded larger outbreaks of the mosquito borne virus in 2007; For the first time, Zika infection also was associated with severe symptoms; including microcephaly in infants infected in the womb; and Guillain Barre syndrome in adults.
But by these acute symptoms and the rapid spread of the virus prompted the World Health Organization to declare Zika a public health emergency of international concern and stimulated interest among scientists in the factors governing Zika infection, about which little is knowing.
In general, flavivirus infection in mammalian cells is mediated by an array of cell surface molecules and attachment cofactors; heat shock protein 70 (Hsp70) is one such host molecule for several viruses; including dengue virus; Japanese encephalitis virus and rotavirus.Hsp70 may act directly as a receptor or indirectly to help attach viruses on the cell surface; where they can interact with specific receptors.
By esting this hypothesis by infecting human liver, human nerve and monkey kidney cells with Zika virus; they using an Hsp70 antibody or a recombinant Hsp70 as a competitor to block the interaction between the protein and the virus; the amount of infectious virus in the cells was reduced, indicating that Hsp70 is involving with Zika virus’s ability to enter cells.
By finding that Hsp70 influences replication of the virus. Their results showed that Zika virus infection induces the expression of Hsp70; and when they treated cells with an Hsp70 inhibitor to reduce production of the protein, it also reduced the production of infectious Zika virus particles. Similarly, when they induced overexpression of Hsp70, production of infectious viral particles was significantly elevating.