A cellular protein appears to enable the infection process of the Zika virus. This protein could be a key target for the development of new therapies to prevent or treat the Zika virus.
The researchers tested their hypothesis by infecting human liver, human nerve, and monkey kidney cells with Zika virus. They found that when they used 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. This finding has indicated that Hsp70 is involved with Zika virus’s ability to enter cells.
Sujit Pujhari, assistant research professor of entomology, College of Agricultural Sciences, Penn State, said: “In these instances, Hsp70 may act directly as a receptor or indirectly to help attach viruses on the cell surface, where they can interact with specific receptors. Hsp70 also plays a role in controlling viral replication in several virus types, including influenza A and rabies. We hypothesized that Hsp70 might have similar functions in relation to Zika.”
Jason Rasgon, professor of entomology and disease epidemiology, Penn State, added: “These findings show that Hsp70 is an integral host molecule for Zika virus infection of host cells, effecting multiple stages of the infection cycle — virus attachment to cells, viral replication inside cells and virus exit from infected cells.”
The Zika virus
Zika is a mosquito-borne virus, which is a member of the Flaviviridae virus family which was first isolated by scientists in 1947. Until recently, it usually only caused mild symptoms in humans. However, larger outbreaks of the virus were recorded in 2007, which culminated in an epidemic in the Western Hemisphere in 2015-16. The Zika infection is now associated with severe symptoms including microcephaly infants infected in the womb, and Guillain-Barre syndrome in adults.
The rapid spread of the virus prompted the World Health Organization to declare Zika a public health emergency of international concern.