FBP1 is a novel positive IRES trans-acting factor that enhances EV71 viral translation and replication, presenting a potential target for antiviral therapy.
Answers are grounded in this paper and cite their sources.
Positions FBP1 as potential EV71 antiviral target in animal models; leaves open human translation and efficacy.
Enterovirus 71 (EV71) is associated with severe neurological disorders in children, and has been implicated as the infectious agent in several large-scale outbreaks with mortalities. Upon infection, the viral RNA is translated in a cap-independent manner to yield a large polyprotein precursor. This mechanism relies on the presence of an internal ribosome entry site (IRES) element within the 5'-untranslated region. Virus-host interactions in EV71-infected cells are crucial in assisting this process. We identified a novel positive IRES trans-acting factor, far upstream element binding protein 1 (FBP1). Using binding assays, we mapped the RNA determinants within the EV71 IRES responsible for FBP1 binding and mapped the protein domains involved in this interaction. We also demonstrated that during EV71 infection, the nuclear protein FBP1 is enriched in cytoplasm where viral replication occurs. Moreover, we showed that FBP1 acts as a positive regulator of EV71 replication by competing with negative ITAF for EV71 IRES binding. These new findings may provide a route to new anti-viral therapy.
No takes yet. Share an insight, caveat, or question.
Huang et al. (2011) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: