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. Author manuscript; available in PMC: 2017 Dec 27.
Published in final edited form as: Virology. 2015 Aug 1;485:116–127. doi: 10.1016/j.virol.2015.07.008

Fig. 7.

Fig. 7

HPgV envelope protein (E2) in extracellular vesicles inhibits IL-12 signaling pathways in NK cells. IFNγ released into NK92MI cell culture supernatants was inhibited following incubation with a range of volumes of HPgV E2 positive or negative extracellular vesicles (EVs) prepared from CHO cell culture supernatants. EVs were quantified by protein-A280 spectrometry. (A). IL-12-mediated signaling of healthy donor peripheral blood mononuclear cells following 18 h incubation with HPgV E2 positive or negative EVs was assessed by intracellular pTyk2, pJak2 and pSTAT4 phosphorylation. HPgV E2 positive EVs inhibited Tyk2 and STAT4 but not Jak2 phosphorylation compared to HPgV E2 negative EV controls (B). Tyk2 phosphorylated HPgV E2 protein in vitro as measured by anti-phosphotyrosine antibodies (C). Two tyrosine residues within HPgV E2 protein (a.a. 85, 87) that are conserved among all 7 HPgV genotypes (representative sequences shown in D) were predicted to interact with a kinase (Tyk2) required for IL-12 induced interferon induction * = p < 0.05, ** = p < 0.01 (T test).