The Crucial Role of Type I Interferons in the Defense Against Viral Infections: Activation of PKR and Induction of Apoptosis

During viral myogenesis, _________ _________________ is produced in infected cells, so the proteins that are made after type I IFNs bind to the infected cells will attach to this structure and the cells will undergo apoptosis and die

During viral myogenesis, double-stranded RNA (dsRNA) is produced in infected cells

During viral myogenesis, double-stranded RNA (dsRNA) is produced in infected cells. This dsRNA acts as a danger signal, indicating the presence of viral infection within the cell. In response to this danger signal, the infected cells release signaling molecules known as type I interferons (IFNs).

Type I IFNs are a group of proteins that play a crucial role in the immune response against viral infections. One of the primary functions of type I IFNs is to activate antiviral defense mechanisms in neighboring uninfected cells. This is achieved by binding to specific receptors on the surface of uninfected cells.

Once type I IFNs bind to their receptors on uninfected cells, a signaling cascade is initiated within these cells. This cascade triggers the expression of various antiviral genes, including those encoding proteins with antiviral properties. One of the key antiviral proteins induced by type I IFNs is protein kinase R (PKR).

PKR is an enzyme that is normally present in cells in an inactive form. However, upon activation by type I IFNs, PKR undergoes a conformational change and becomes active. Active PKR then phosphorylates (adds a phosphate group to) a protein called eukaryotic initiation factor 2 alpha (eIF2α).

eIF2α is an essential component of the protein translation machinery within cells. When eIF2α is phosphorylated by activated PKR, it inhibits the initiation of protein synthesis, thereby shutting down global protein production in the infected cell. This mechanism helps to prevent the synthesis of viral proteins and impairs the replication and spread of the virus within the host.

Additionally, the shutdown of protein synthesis induced by type I IFNs and activated PKR can lead to stress within the infected cell. This stress response ultimately triggers programmed cell death, also known as apoptosis. Apoptosis is a tightly regulated process that results in the orderly and controlled dismantling of the infected cell, preventing further viral replication and spread.

In summary, during viral myogenesis, dsRNA is produced in infected cells, leading to the release of type I IFNs. When type I IFNs bind to uninfected cells, they activate PKR, which in turn inhibits protein synthesis and induces apoptosis. This mechanism serves as an important defense mechanism by eliminating infected cells and limiting the spread of viral infection.

More Answers: