FIG 1 .

wStri inhibits DENV and ZIKV but not LACV or VSV. Wolbachia wStri-infected A. albopictus cells (W+) and uninfected Wolbachia-free control (W−) cells were infected with DENV-2, ZIKV, YFV 17 D, CHIKV, LACV, or VSV at an MOI of 10. After 3 days, virus supernatant was collected and infectious virus was assessed in a focus-forming assay (DENV and YFV) or plaque-forming assay (ZIKV, CHIKV, LACV, and VSV). Data shown are means and standard deviations of results from three independent experiments for each virus. (A) Positive-sense RNA virus genomes; (B) negative-sense RNA virus genomes. Statistical differences were determined with Student’s t test for each experiment. Where distribution of data was nonnormal due to no virus detected (YFV), the data were log transformed prior to the t test. P values were as follows: YFV, P = 0.003; DENV, P = 0.00004; ZIKV, P = 0.001; CHIKV, P = 0.003; LACV, P = 0.24; VSV, P = 0.26. (C) Wolbachia wStri-infected A. albopictus cells (W+) and uninfected Wolbachia-free control (W−) cells were infected with ZIKV at an MOI of 10. Filtered medium from the spent W− culture or from the spent W+ culture was added to infected cells. Three days postinfection, cell supernatants were harvested and viral growth was assessed by plaque assay. *, P < 0.05.