FIG 5.
Introduction of LCMV Z NTD to the nonpathogenic PICV genome allows Z-RLR binding in the infected cells and increases viral replication in macrophages. (A) LCMV Z NTD mediates the interaction with endogenous RIG-i and MDA5 in virus-infected cells. The hMDMs were infected with the respective arenaviruses at MOI of 5. Cell lysates were immunoprecipitated with rabbit IgG, rabbit anti-RIGi, or rabbit anti-MDA5 antibodies and detected by anti-RIGi antibody, anti-MDA5 antibody, or anti-Z antibody, respectively. WB, Western blotting. (B) Similar viral growth kinetics of rP18-ZNLCMV and the parental rP18 in Vero cells infected at MOI of 0.01. (C) Viral titers at 24 hpi from hMDMs infected (MOI = 1) with LCMV, TCRV, PICV P2, PICV P18, or rP18-ZNLCMV. Results shown represent the averages of the results of three independent experiments, each performed using PBMCs from a different donor. Statistical analysis was conducted using the Student t test. **, P < 0.01; *** P < 0.001; ns, not statistically significant.