Skip to main content
. 2010 Jul 29;6(7):e1001001. doi: 10.1371/journal.ppat.1001001

Figure 2. The MAVS-IKKβ pathway is necessary for efficient γHV68 lytic replication ex vivo.

Figure 2

(A) Two known pathways, the IKKα/β/γ-NFκB and TBK-1/IKKε-IRF pathways, downstream of MAVS. (B) The initiation of γHV68 lytic replication in wild-type (WT) MEFs and MAVS−/−, IKKα−/−, IKKβ−/−, IKKγ−/−, TRAF6−/−, IFNAR−/−, and IRF3−/−IRF7−/− (double knockout) MEFs was assessed by a plaque assay. Data represent the mean ± SEM of three independent experiments. (C) Multi-step growth properties of γHV68 (MOI = 0.01) in wild-type MEFs and IKKβ−/−, IKKγ−/−, and IKKα−/− MEFs were examined by plaque assays. Data represents three independent experiments. (D to F) Wild-type, MAVS−/−, and IKKβ−/− MEFs were respectively infected with control lentivirus (Vec) or lentivirus containing the Flag-tagged IKKβ (IKKβ), and selected with puromycin. (D) IKKβ expression was confirmed by immunoprecipitation and immunoblot with anti-Flag antibody (top). γHV68 plaque assays were performed as in (B). (E) Reconstituted MEFs of indicated genotypes were used for γHV68 plaque assays as in (B) with increasing doses of γHV68. Data represent the mean ± SEM of three independent experiments. (F) Reconstituted IKKβ−/− MEFs as indicated were infected with γHV68 K3/GFP (MOI = 0.01), and viral multi-step growth was determined by a plaque assay. Statistical significance (P-value) in (B), (D), and (E) was calculated with two-tailed unpaired Student's t-test: *, P<0.05; **, P<0.02; ***, P<0.005.