Scientists have got great success on Lassa virus. US researchers have identified the role of a protein that plays a key role in the progression of Lassa fever. It has been observed mainly in West Africa. Lassa fever is an acute viral hemorrhagic disease similar to Ebola, which is transmitted to people through contact with food or other objects that have been contaminated with the urine or feces of infected mice.
Although it has a mortality rate of 15 percent in severe cases, up to 90 percent in pregnant women, and deafness in up to a quarter of survivors, there is no vaccine or antiviral to protect against Lassa virus. To save lives, scientists at the La Jolla Institute for Immunology (LJI) and Scrapcy Research are working to understand how the Lassa virus replicates within human hosts.
Increases infection by using cellular proteins
In a new study published in the Proceedings of the National Academy of Sciences, researchers show how a key Lassa virus protein, called a polymerase, drives infection in human hosts using a cellular protein. Jingru Fang, a joint LJI and Scrapsi Research graduate student, explains that there is no antiviral drug that specifically targets the Lassa virus.
Fang said that is why it is important for researchers to identify potentially drugable targets on this virus to combat infection. Lassa virus encodes only four viral proteins. One of them, the polymerase, directs the process of virus genome replication and gene expression to produce material the virus spreads to new host cells. The researchers led the discovery of host cellular proteins that could act as partners of LasA polymerase.
Host protein GSPT1 linked to virus infection
This study is the first to uncover the molecular cross-talk between Lassa virus polymerase and cellular proteins. However, this is the second time the host protein GSPT1 has been linked to virus infection. “If we can find a way to inhibit the link between GSPT1 and Lassa polymerase, or if we can simply remove the GSPT1 protein, we can stop Lassa virus infection,” Fang said. ‘