FIG. 5.

Efficacy of anti-NS1 MAbs in wild-type, C1q-deficient, or Fc γ receptor I- and III-deficient mice. (A) C1q-deficient or (B) Fc γ receptor I- and III-deficient mice were inoculated subcutaneously with 10² PFU of WNV at day zero. At the same time, mice were administered PBS or a single dose of 14NS1, 16NS1, or 17NS1 via an intraperitoneal route. The number of animals for each antibody dose ranged from 15 to 27. The difference in survival curves was statistically significant for all WNV NS1-specific monoclonal antibodies shown in the C1q-deficient mice (P ≤ 0.0004). The difference in survival curves for the Fc γ receptor I- and III-deficient mice was significant for MAb 14NS1 (P = 0.003) and 16NS1 (P = 0.04) but not for 17NS1 (P = 0.3). (C and D) Therapeutic activity of MAbs 14NS1 and 16NS1. At day 2 (C) or 4 (D) after WNV infection, 5-week-old C57BL/6 mice were passively transferred saline or a single intraperitoneal inoculation of 14NS1, 16NS1, or 14NS1 plus 16NS1 as ascites fluid. The survival curves were constructed with a total of 10 to 20 mice for each treatment group. The statistical difference in survival curves compared to saline was as follows: day 2, mice treated with 14NS1 (P = 0.0003), 16NS1 (P < 0.0001), or 14NS1 plus 16NS1 (P = 0.0001); day 4, mice treated with 14NS1 (P > 0.1), 16NS1 (P = 0.03), or 14NS1 plus 16NS1 (P = 0.02). An arrow shows the timing of MAb administration.