FIG 8.

Proposed model for AIMP2 as a positive regulator of influenza virus replication. AIMP2 is incorporated into the ARS complex under physiological conditions. Following IAV infection, AIMP2 dissociates from the ARS complex and the released AIMP2 can be ubiquitinated by Parkin or another E3 ligase for degradation. To prevent ubiquitin-mediated degradation of AIMP2, NS2 is able to interact with AIMP2 to keep it away from ubiquitination. Following binding with NS2, AIMP2 recruitment prevents K242-mediated ubiquitination and degradation of M1. M1 then translocates into the nucleus, where it is SUMOylated at K242. The SUMOylation of M1 facilitates the formation of the NS2-M1-vRNP complex, modulates the nuclear export of vRNPs, and promotes the assembly and budding of progeny virions.