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. Author manuscript; available in PMC: 2024 Feb 1.
Published in final edited form as: Neuron. 2022 Sep 28;110(23):3936–3951.e10. doi: 10.1016/j.neuron.2022.09.002

Figure 5. Glioma myeloid cells confer ZIKV resistance.

Figure 5

(A) Primary GBM samples were dissociated to single-cell suspension and plated in bulk (GBM), or first separated into CD11b-enriched (GBM11b+) and CD11b-deplete fractions (GBM11b-) using antibody-conjugated magnetic bead and column-based sorting. These fractions were assayed directly, or in coculture with HDB and GBM lines.

(B) Representative IF images of SOX2+ glioma cells and IBA1+ myeloid cells in GBM, GBM11b+ and GBM11b-fractions, and average proportion of each cell type across n=4 matched bulk and sorted GBM fractions.

(C) ZIKV PE243 copy number assayed by RT-qPCR in paired infected GBM and GBM11b+ primary cultures (n=3).

(D) ZIKV PE243 copy number assayed by RT-qPCR in paired infected GBM and GBM11b-primary cultures (n=3).

(E) GBM E22 line infected in isolation, or in coculture with GBM11b- or GBM11b+ fractions at a 2:1 ratio, then fixed at 48 h.p.i. for IF (See also Figure S5).

(F) GBM E22 line infected in isolation, or in coculture with GBM11b- or GBM11b+ fractions, processed for RNA extraction and RT-qPCR viral copy number assay (unpaired t-test *p<0.05; ** p<0.01; ***p<0.001) (See also Figure S5).