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. Author manuscript; available in PMC: 2017 Dec 4.
Published in final edited form as: Science. 2017 Mar 30;356(6334):175–180. doi: 10.1126/science.aal4365

Fig. 2. Enhancement of ZIKV infection through IgG engagement of Fcγ receptors.

Fig. 2

(A) IgG purified from plasma pooled (n = 15 per group) from control, DENV-, or WNV-infected donors was evaluated for enhancement of ZIKV infection in K562 cells. (B) Pooled plasma samples from control, DENV-, or WNV-infected donors were evaluated for enhancement of ZIKV infection in K562 cells before and after IgG purification. (C to E) Purified IgG from control, DENV-, or WNV-seropositive donors was tested for enhancement of ZIKV infection in K562 cells in the presence or absence of Fcγ receptor binding inhibitor (FcγR BI) (C), antibodies (α) against CD32 (D), or antibodies against CD16 (E). (F) Plasma IgG from control, DENV-, or WNV-seropositive donors was incubated in the presence or absence of PNGase F before evaluation of ZIKV infection enhancement in K562 cells.The same control, DENV, and WNV IgG samples are shown in (A), (C), (D), and (E). All graphs show means ± SD.