Background
Type I interferons (IFNs) stimulate the establishment of an antiviral state in infected and susceptible cells and play a key role in the initial containment of many virus infections. Most viruses have evolved at least one strategy for the evasion of this antiviral response. The acute burst of viral replication in primary HIV-1 infection is associated with a transient elevation in systemic IFN-alpha levels. This study addressed the relationship between acute-phase viral sensitivity to type I IFNs in vitro and the prognostically-important setpoint persisting viral load established in subjects with primary HIV-1 infection.