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

Figure 1. MAVS deficiency reduces γHV68 lytic replication.

Figure 1

MAVS wild-type (MAVS+/+) or knockout (MAVS−/−) mice were intranasally (i.n.) infected with 40 PFU γHV68. The lungs were harvested at 4, 7, 10, 13, and 16 days post-infection (d.p.i.) and viral titer was determined by a plaque assay. (B) Mouse embryonic fibroblasts (MEFs) were infected with a GFP-marked γHV68 K3/GFP at multiplicities of infection (MOI) of 0.01. Viral replication in MAVS+/+ and MAVS−/− MEFs were photographed. (C) MEFs were infected with γHV68 K3/GFP as in (B) and viral titers were determined by a plaque assay. Data represent three independent experiments and error bars denote standard error of the mean (SEM). (D) MAVS+/+ and MAVS−/− MEFs were infected with 120 PFU γHV68 K3/GFP or 5 PFU vesicular stomatitis virus (VSV), and plaques were counted. Data represent the mean ± SEM of three independent experiments. (E to G) MAVS−/− MEFs were respectively infected with control lentivirus (Vec) or lentivirus containing the Flag-tagged human MAVS (MAVS), and selected with puromycin. (E) MAVS expression was confirmed by immunoprecipitation and immunoblot with anti-Flag antibody. (F) γHV68 plaque assays were performed as in (D). (G) Reconstituted MAVS−/− 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 in (A), (D), and (F): *, P<0.05; **, P<0.02; ***, P<0.005.